Rare Gene Increases Cancer Risk: 100% Chance of Developing Cancer Explained

Posted on June 26, 2026 by Igor Mitreski

Tracy Hutchinson has a rare mutation in the TP53 gene

Tracy Hutchinson

When several family members were diagnosed with cancer simultaneously, I began to suspect a hereditary issue. In 1990, my sister Rebecca and I were both diagnosed with acute lymphoblastic leukemia—she was 21, and I was just 14. During her intense chemotherapy treatment, our mother was also diagnosed with breast cancer.

Tragically, Rebecca passed away in 1994, and not long after, my father was diagnosed with colon cancer. As he was receiving treatment, my grandmother was diagnosed with cancer in her other breast, which she survived, only to be later diagnosed with esophageal cancer in 2009. Despite undergoing major surgery, my father’s cancer recurred, and he succumbed to the disease six weeks later.

In 2020, when my other sister was diagnosed with rapidly progressing triple-negative breast cancer, I thought, “Oh my God, something is definitely wrong.” She was tested for the BRCA mutation and results showed no BRCA1 or BRCA2 mutations. Subsequently, she was tested for a rarer mutation in the TP53 gene. This mutation is linked to a significantly heightened cancer risk. Women with this mutation have an almost 100% likelihood of developing some form of cancer during their lifetime. This genetic condition is known as Li-Fraumeni syndrome, which indicates that the TP53 genes, responsible for tumor suppression, are not functioning properly.

When my sister suggested I get tested, I questioned, “What is Li-Fraumeni syndrome?” I had never heard of it before. Discovering my positive test result was emotionally devastating, but I agreed to undergo testing to support my sister during this challenging time.

In 2022, at the age of 47, I received my positive diagnosis. Surprisingly, I felt a sense of comfort knowing that I had answers regarding the struggles my family faced. However, this revelation was deeply personal; for example, my brother opted not to be tested.

After my diagnosis, my life transformed completely. With Li-Fraumeni syndrome, thoughts of cancer are ever-present. Within months of learning my result, I underwent a preventive double mastectomy. Early-stage cancer, specifically ductal carcinoma in situ, was detected in my left breast after the surgery.

Living in Sydney, I enrolled in an Australian clinical trial investigating the use of annual full-body MRIs for early tumor detection in individuals with TP53 mutations or other cancer-associated genes. In 2022, I welcomed my first baby, but during my second year, a 9-millimeter meningioma was discovered—fortunately benign but nonetheless terrifying.

I receive full-body MRIs annually, but my anxiety peaks around July, as I wonder if this will be the year things take a turn for the worse. Participating in this study provides some reassurance, as it aims to catch cancer at an early, treatable stage. My sister, who survived breast cancer, also undergoes yearly MRIs.

In addition to full-body MRIs, I have annual skin exams and blood tests managed by a dermatologist. Bi-yearly endoscopies and colonoscopies are essential; during one procedure, they discovered and removed a polyp in my intestine and atypical cells in my esophagus, which are now closely monitored. I’m vigilant about any irregularities in my body—any sudden shoulder pain sends my anxiety into overdrive.

My geneticist speculated that our mother may have had a spontaneous mutation in the TP53 gene, instead of it being inherited. As neither my sister nor I have children, the risk of passing this mutation on is nonexistent.

My partner has been incredibly supportive. After my diagnosis, he encouraged me to pursue whatever necessary actions I needed to take. When I opted for a double mastectomy without reconstruction, he reassured me, saying my scars tell the story of my journey.

I strive to maintain a positive outlook despite the challenges, aware that everyone faces their own struggles, whether chronic illnesses or hidden mental health battles. For instance, my sister-in-law recently suffered a stroke. We each carry our own burdens, visible or not, and it’s crucial to be compassionate toward one another; life isn’t always picture-perfect.

As told by Alice Klein

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Source: www.newscientist.com

Breakthrough Discovery: Antarctic Creature May Pave the Way for Cancer Treatment Advances

Posted on June 26, 2026 by Igor Mitreski

The potential cure for skin cancer may originate from one of the most isolated and inhospitable regions on our planet.

Recent studies have revealed that a species of sea squirt found in Antarctica produces bacteria that harbor toxic compounds capable of targeting and killing melanoma cells, while leaving healthy human cells unharmed.

“Selectivity is crucial in drug development, as our goal is to treat the disease without harming the patient,” says Bill Baker, a chemistry professor at the University of South Florida (USF) and co-leader of this groundbreaking research.

An estimated 57,000 individuals die annually from melanoma, the most severe type of skin cancer, and projections suggest this number could rise to 96,000 by 2040.

The highest incidence rates are observed among fair-skinned populations in countries like Australia and New Zealand, as well as Western Europe, yet innovative treatments may be found further south.

Sea squirts, also known as tunicates, are pouch-shaped marine invertebrates that inhabit the sloping floors of the ocean.

Antarctic wildlife, like many organisms on the continent, has evolved over millions of years to withstand extreme conditions, developing unique chemical defenses against predators and disease.

The USF research team, alongside scientists from the Desert Research Institute and the Scripps Institution of Oceanography, dedicated six weeks to exploring Antarctic waters, diving approximately 80 feet below the ice—a mission that posed challenges such as shifting oceans, poor visibility, and encounters with leopard seals.

Researchers may be on land, but their studies on sea squirts continue—Credit: Sam Affoullous, USF

Currently, researchers are analyzing the DNA, chemistry, and biology of these ascidians, a comprehensive process that may take years to yield results.

“This research is vital for both environmental and medical purposes,” Baker stated. “Understanding the source and function of this compound is essential to its development as a therapeutic agent.”

Sea squirts aren’t the only unusual organisms providing insights into cancer treatment. For instance, naked mole rats, despite their unconventional appearance, appear to be entirely immune to cancer, although the underlying reasons remain unclear.

Additionally, researchers in the United States have identified compounds in scorpion venom that show promise in combating aggressive brain tumors.

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Source: www.sciencefocus.com

How Phages Could Hijack Vaccine Immunity to Target and Destroy Cancer Cells

Posted on June 25, 2026 by Igor Mitreski

Transmission Electron Micrograph of E. coli Infected with Phage (Green Dots)

M. Mader/Department of Microbiology, Biozentrum/Science Photo Library

Transmission electron micrograph of E. coli cells infected with phage (green dots) — Transmission Electron Micrograph of E. coli Infected with Phage (Green Dots)

M. Mader/Department of Microbiology, Biozentrum/Science Photo Library

A groundbreaking study reveals that bacteriophages, viruses that target bacteria, can help in eliminating cancer cells by reorienting the immune response established through vaccination. In experiments involving mice vaccinated against malaria, a harmless phage was utilized to target and eradicate tumors, achieving success in nearly 44% of the subjects.

Immunotherapy has revolutionized cancer treatments, yet many patients do not reap its benefits due to the challenge of getting the immune system to identify tumors as threats. To address this,
Amin Hajitou and his team from Imperial College London investigated phages that specifically infect
Escherichia coli. These phages attach to bacteria, inject their genetic material, and replicate, thereby destroying the bacterial cells.

The research team engineered the phages to specifically target proteins known as αvβ3 and αvβ5 integrins, which are prevalent in tumor cells but scarce in healthy cells. Additionally, they customized the phages to produce malaria-specific antigens—signals that prompt the immune system to recognize them as foreign invaders. “Phages function as targeted delivery vehicles,” explains Hajitou.

The efficacy of this approach was tested on 60 mice with subcutaneous tumors. Among them, 15 mice received a malaria vaccine followed by injections of engineered phages at two-week intervals. The control group consisted of 15 mice each receiving no treatment, the malaria vaccine only, or the engineered phage exclusively.

The results revealed that tumors disappeared in 44% of the treated mice, with no recurrence observed a year post-study. Although the treated mice exhibited longer lifespans compared to controls, a survival advantage was not significantly noted.

According to
David Withers at Oxford University, “These engineered viruses can target and infect tumor cells systemically.” This strategy marks a significant advancement over current methods of manipulating tumors, such as oncolytic viruses, which necessitate direct injections at cancer sites—an impractical method especially for metastatic diseases.

By fine-tuning the phage’s antigen-producing capabilities, this innovative approach could also extend its effectiveness to individuals vaccinated against other infectious diseases like seasonal influenza and COVID-19, showcasing the versatility of this method. Hajitou asserts, “More potent vaccines than malaria are likely to yield even greater results.” The aim is to leverage existing immune memory without being limited to malaria-specific responses.

The research team is currently engaging with the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) to explore the possibility of commencing early-stage human trials next year.

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Source: www.newscientist.com

Phage Therapy: Harnessing Viral Power to Enhance Vaccine Immunity and Target Cancer Cells

Posted on June 25, 2026 by Igor Mitreski

Transmission Electron Micrograph Reveals E. coli Cells Infected by Phage (Green Dots)

M. Mader/Department of Microbiology, Biozentrum/Science Photo Library

A groundbreaking study reveals that a bacteria-killing virus can selectively destroy cancer cells in mice. By harnessing the immunity generated from vaccination, researchers redirected the immune response to effectively target and eradicate tumors. In trials, nearly 50% of vaccinated mice infected with a harmless phage demonstrated tumor disappearance.

Immunotherapy has revolutionized cancer treatment, but many still struggle to benefit due to challenges in immune system recognition of tumors. The latest research aims to enhance this recognition.

Researchers led by Amin Hajitou at Imperial College London investigated phages that infect Escherichia coli. Upon infecting the bacteria, these phages inject genetic material, reprogramming the bacterial machinery to generate numerous new phages that effectively eradicate these pathogens.

To improve targeting, the team genetically engineered the phages to recognize proteins called αvβ3 and αvβ5 integrins, which are prevalent in many tumor cells but are scarce in healthy tissues. Additionally, they modified the phage’s genetic payload to include malaria-specific antigens to stimulate a robust immune response. “Phages serve as precision delivery vehicles for our interventions,” states Hajitou.

The researchers conducted tests on 60 mice with tumors positioned under the skin. A subset received a malaria vaccine, followed by phage injections in the tail over two weeks. Control groups included those receiving no treatment, only the vaccine, or only the engineered phage.

Results showed that tumors vanished in 44% of treated mice, and notably, these tumors did not recur a year post-study. Additionally, treated mice exhibited increased lifespans compared to their untreated counterparts, though no significant survival advantage was observed.

“This innovative approach allows engineered viruses to systematically target tumor cells,” remarks David Withers from Oxford University. “This capability markedly enhances current strategies for manipulating tumors, such as using oncolytic viruses, which are limited by the need for direct administration into cancer sites.”

With further adjustments to the phage’s antigen-producing capabilities, the technique may also apply to humans vaccinated against diseases like seasonal influenza and COVID-19. “Utilizing more effective vaccines than malaria could amplify our results,” Hajitou explains. “This strategy leverages pre-existing immune memory and is not confined to malaria alone.”

The research team is currently in discussions with the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) to initiate early-stage human trials as soon as next year.

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Source: www.newscientist.com

How the HPV Vaccine Significantly Lowers Cervical Cancer Death Rates

Posted on June 18, 2026 by Igor Mitreski

The HPV vaccine has revolutionized cervical cancer prevention since its launch in 2006

Subhash Shrestha/Nuru Photography via Getty Images

Between 2020 and 2024, there have been no cervical cancer deaths among women aged 20 to 24 in the UK. This unprecedented milestone is attributed to the effective rollout of HPV vaccines.

“The results are remarkable,” says Peter Sasieni from Queen Mary University of London. “It’s tragic when young women succumb to cervical cancer. The rapid deployment of the vaccine is a monumental triumph for vaccination, science, and public health.”

Various types of HPV are sexually transmitted and can lead to cellular changes that increase cancer risk. HPV-related cervical cancer can develop in women as young as their 20s, and globally, many still die from this disease.

The initial HPV vaccine was launched in 2006, and girls aged 12-13 in the UK have been vaccinated since 2008. In 2019, vaccination programs for boys were initiated to help prevent other HPV-related cancers, such as mouth, anal, throat, and penile cancers, while also reducing the spread of the virus.

This study serves as the first robust evidence that the HPV vaccine significantly lowers the rates of HPV infection and cervical cancer mortality. Research on cervical cancer incidence supports this assertion. Although it may seem straightforward to prevent deaths, Sasieni emphasizes that women less likely to get vaccinated also tend to miss screenings. This raised concerns that vaccines primarily protect those cancers detectable through early screening, rather than the more aggressive cancers that screening might miss.

Fortunately, this is not the case. Sasieni and his colleague Milena Falcaro have been tracking cervical cancer statistics in the UK and found no deaths among women aged 20 to 24 from 2020 to 2024, based on the latest data. Historically, about 23 deaths were expected. “I’ve never seen a year with zero deaths,” Sasieni remarked, “so five consecutive years without any is truly remarkable.”

This significant reduction is likely due to the HPV vaccination, with around 90% of women aged 20-24 in the UK having been vaccinated at age 12 or 13. “This promising information reveals that the HPV vaccine saves lives, allowing us to confidently tell this generation that cervical cancer and other cancers related to HPV are not a threat,” says Caroline Temmink, Director of Vaccination at NHS UK.

While this study primarily focused on cervical cancer, the HPV vaccine also targets other HPV-related cancers, benefiting both men and women by preventing genital warts.

Sasieni and Falcaro did note deaths among women aged 25 to 29, but these were significantly lower than anticipated. In total, they estimate that approximately 200 lives have already been saved, which is only the beginning. “The 200 lives estimated is only the surface, as it appears to provide long-term protection,” Sasieni stated. “In the future, we may project around 18,000 deaths that could be prevented due to the vaccine.”

However, the global coverage of the HPV vaccine remains low, and cervical cancer rates are still rising. There are concerns that death rates could increase as fewer teenagers receive vaccinations in the UK. “The concerning fact is that vaccine uptake has significantly dropped since COVID-19,” Sasieni warned.

“HPV vaccination remains crucial to the NHS’s goal of eradicating cervical cancer by 2040,” notes Temmink. “This safe and effective vaccine should be embraced by everyone eligible when offered.”

Topic:

Source: www.newscientist.com

Why No Young Woman Has Died from Cervical Cancer in the UK for Many Years

Posted on June 18, 2026 by Igor Mitreski

HPV Vaccines: A Game Changer in Cervical Cancer Prevention Since 2006

Subhash Shrestha/NurPhoto via Getty Images

From 2020 to 2024, no women aged 20 to 24 in the UK succumbed to cervical cancer, marking the first instance of zero deaths in this age group. This milestone is attributed to the rollout of vaccines against the human papillomavirus (HPV).

“The findings are remarkable,” states Peter Sasieni from Queen Mary University of London. “It’s heartbreaking when young individuals die from cervical cancer. The rapid vaccine rollout symbolizes a triumph for vaccination, science, and public health.”

Numerous strains of HPV are sexually transmitted and can alter cells in ways that significantly increase cancer risk. Consequently, cervical cancer can arise in women as young as their 20s, and many continue to die from it worldwide.

Since the first HPV vaccine was introduced in 2006, adolescent girls in the UK have been vaccinated since 2008, with boys starting in 2019. This initiative not only protects against cervical cancer but also prevents other HPV-related cancers such as those of the mouth, throat, anus, and penis, mitigating the transmission of the virus.

This research serves as the first robust evidence indicating that the HPV vaccine not only substantially decreases HPV infections but also prevents fatalities related to cervical cancer. Cervical cancer incidence could potentially be decreasing faster than expected. Previous concerns suggested that the vaccine primarily prevented cancers detected early through screenings, but it appears to be effective for cancers that screening missed as well, according to Sasieni.

Fortunately, this is not the case. Sasieni and his colleague Milena Falcaro have been tracking cervical cancer rates in the UK, revealing zero deaths among women aged 20 to 24 from 2020 to 2024. Historical data suggested about 23 deaths were expected within this age group. “Never has there been a year with zero deaths, so five consecutive years is incredibly impressive,” Sasieni noted.

The substantial decrease in cases is likely due to the HPV vaccine, with approximately 90% of women aged 20 to 24 in the UK receiving the vaccine at 12 or 13. “This encouraging news demonstrates that the HPV vaccine is lifesaving,” stated Caroline Temmink, Director of Vaccination for the UK National Health Service (NHS). “We are excited to tell this generation: ‘Cervical cancer and several other cancers are no longer a risk for you.'”

While this particular study focused on cervical cancer, the vaccine offers protection against other HPV-related malignancies as well, significantly reducing the risk of warts in the skin, genitals, and anal region.

Sasieni and Falcaro also acknowledged some fatalities occurring in women aged 25 to 29, but the figures were notably lower than anticipated. They estimate that around 200 lives have already been saved, which is just the beginning. “The 200 lives estimated in the paper is merely the tip of the iceberg, as it appears to provide long-term protection,” Sasieni remarked. “In the future, nearly 18,000 deaths may be a rough estimate of those we’ve prevented so far.”

However, worldwide HPV vaccine coverage remains low, and the incidence of cervical cancer is increasing. Concerns arise as vaccination rates among teenagers in the UK have dropped post-COVID-19. “The alarming news is that vaccine uptake has declined significantly since the pandemic,” Sasieni warned.

“Together with cervical cancer screenings, HPV vaccinations are central to the NHS’s goal of eradicating cervical cancer by 2040,” says Temmink. “This is a safe and effective vaccine, and we urge all eligible individuals to take up the opportunity when invited.”

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Source: www.newscientist.com

Link Between E-Cigarette Use After Quitting Smoking and Lung Cancer Risk

Posted on June 12, 2026 by Igor Mitreski

Increasing Evidence of E-Cigarette Health Risks

Image Credit: Dead Mitiei/Shutterstock.

E-cigarettes health risks — Increasing Evidence of E-Cigarette Health Risks

Image Credit: Dead Mitiei/Shutterstock.

A recent study involving over 4.5 million participants indicates that smokers who switch to vaping after quitting cigarettes are more than 50% more likely to develop lung cancer compared to those who successfully quit smoking altogether. However, it still underscores that e-cigarettes may present less risk than continuing to smoke.

“This study contributes to a growing body of evidence indicating that e-cigarettes are not as low-risk as previously believed,” says Becky Freeman from the University of Sydney, Australia, who was not involved in the research. “[It’s] crucial for those attempting to quit smoking to seek safer options first, and only use e-cigarettes after exhausting other methods.”

In the UK by 2024, over 40% of smokers who quit are expected to use e-cigarettes. Notably, 20% of ex-smokers were still vaping more than a year after quitting. Although many advocate for e-cigarettes as an effective smoking cessation tool, they have been associated with airway inflammation, reduced lung function, and even lung cancer in animal studies.

To further investigate the effects of e-cigarettes, Kim Young Wook and researchers from Seoul National University followed more than 4.5 million adult smokers as part of South Korea’s National Health Checkup Program from 2018 to 2023.

Participants were categorized as current smokers, short-term quitters (those who hadn’t smoked since at least 2018), or long-term quitters (those who hadn’t smoked since at least 2014). Over the study period, 35,887 participants developed lung cancer, with 12,807 related deaths recorded.

Analysis of this data revealed that ex-smokers who vape are at a significantly greater risk of lung cancer death compared to their counterparts who stopped smoking completely. “Ex-smokers who continued vaping faced a 56% higher risk of lung cancer,” Kim stated.

While long-term studies are essential, some chemicals found in e-cigarettes have been associated with DNA damage. Vaping has also been linked to oxidative stress, meaning an imbalance between free radicals and antioxidants in the body, as well as epigenetic changes affecting genes and inflammation of respiratory and oral tissues.

Nonetheless, Kim and his team emphasize that they cannot definitively conclude that e-cigarettes cause lung cancer, and that further research is warranted, especially in populations outside of South Korea.

Remarkably, ex-smokers who vape experienced a significantly lower risk of death from all causes in comparison to active smokers, reinforcing the broader health benefits of quitting smoking altogether.

Nicole Lee from Curtin University in Perth, Australia, pointed out that the study’s findings suggest that completely quitting both smoking and vaping is more effective for preventing lung cancer than continuing to vape while attempting to quit smoking. “The results of this study are vital for individuals who have quit smoking,” she emphasized.

“Our recommendation to smokers remains that the safest choice is to quit entirely, but if quitting is challenging, [without the use of e-cigarettes] or if they prefer not to use them, transitioning to e-cigarettes is a safer alternative,” Lee stated. “As a harm reduction strategy, it certainly is preferable to continuing to smoke.”

Professor Bernard Stewart from the University of New South Wales in Sydney added that further research is necessary before implementing public health policies that may impose additional restrictions on e-cigarettes.

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Source: www.newscientist.com

Reducing Cancer Risks: How Quitting Cigarettes and Vaping Can Mitigate Smoking’s Impact

Posted on June 11, 2026 by Igor Mitreski

Emerging Evidence: E-Cigarettes and Health Risks

Credit: Dead Mitiei/Shutterstock.

A groundbreaking study involving over 4.5 million participants reveals alarming statistics: smokers who switched to vaping post-cessation face more than a 50% increased risk of developing lung cancer compared to those who quit smoking entirely. Nonetheless, the research also emphasizes that using e-cigarettes to aid in quitting is a safer alternative than continued cigarette smoking.

As noted by Becky Freeman from the University of Sydney, Australia, who was not part of the study, “This research contributes to a growing body of evidence indicating that e-cigarettes may not be as low-risk as initially suggested. It’s essential for those attempting to quit smoking to explore safer options, yet effective cessation methods should be prioritized first.”

In the UK, over 40% of smokers are expected to use e-cigarettes in 2024, with 20% of ex-smokers continuing to vape over a year after quitting. Although e-cigarettes are often praised as a cessation tool, research links them to airway inflammation, diminished lung function, and increased cancer risk in animal studies.

To delve deeper into the effects of e-cigarettes, Kim Young Wook and a team from Seoul National University analyzed data from South Korea’s National Health Checkup Program from 2018 to 2023, tracking participants classified as current smokers, short-term quitters, or long-term quitters. Throughout the five-year span, 35,887 individuals developed lung cancer, leading to 12,807 related deaths.

Upon analyzing e-cigarette usage among different participant groups, researchers discovered that ex-smokers who continued to vape exhibited a significantly higher risk of dying from lung cancer compared to non-vapers. “Those who used e-cigarettes after quitting had a 56% elevated risk when compared to individuals who quit smoking completely,” Kim noted.

While the need for extended research is clear, certain studies suggest that e-cigarette chemicals may cause DNA damage, and vaping has been associated with oxidative stress, epigenetic changes, and inflammation in respiratory and oral tissues.

However, Kim’s team emphasizes that causation cannot be definitively established, stressing the necessity for further investigations, particularly involving diverse populations outside South Korea.

Remarkably, it was found that ex-smokers who utilized e-cigarettes had a significantly lower overall mortality risk compared to current smokers, reinforcing the substantial health benefits of quitting smoking altogether.

According to Nicole Lee from Curtin University in Perth, Australia, the study underscores that quitting both smoking and vaping entirely is more effective in preventing lung cancer than merely transitioning to e-cigarettes during the quitting phase. “The implications of this study are crucial for those who have stopped smoking,” she stated.

“Our ongoing recommendation to smokers is that complete cessation is the safest option. However, if quitting is unachievable for some, switching to e-cigarettes is certainly a less harmful alternative compared to continued smoking,” Lee advised.

Lastly, Bernard Stewart, a professor at the University of New South Wales in Sydney, emphasized the need for further research before implementing public health policies that may introduce additional e-cigarette regulations.

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Source: www.newscientist.com

Breakthrough Pancreatic Cancer Drug Doubles Survival Rates: A Revolutionary Treatment

Posted on June 2, 2026 by Igor Mitreski

Daraxone Lasib: An Innovative Approach for Advanced Pancreatic Cancer Treatment.

Credit: Reuters/Danielle Villasana

Daraxone Lasib: A Revolutionary Drug for Advanced Pancreatic Cancer — Daraxone Lasib: An Innovative Approach for Advanced Pancreatic Cancer Treatment.

Credit: Reuters/Danielle Villasana

Daily administration of Daraxone Lasib has shown potential to double survival rates for pancreatic cancer patients, especially when conventional chemotherapy has ceased to be effective. This oral medication is associated with significantly fewer side effects compared to traditional chemotherapy treatments.

“This represents a breakthrough in treatment,” states Pilar Acedo of University College London, who was not part of this research. “For years, the survival statistics of pancreatic cancer have been bleak. With this new treatment, patients can expect to spend twice as long enjoying life, with loved ones.”

About 70% of pancreatic cancer cases are diagnosed at an advanced stage, primarily due to irregular medical check-ups and ambiguous symptoms like back pain, leading to late-stage discovery. Conventional chemotherapy remains the standard approach; however, the average survival time for most patients is merely three to six months. Acedo noted, “This cancer is incredibly aggressive and challenging to manage.”

Over 90% of pancreatic cancers arise from mutations in the K-Ras gene, resulting in abnormal cell proliferation. This alteration in gene function has significant implications for cancer progression.

Eileen O’Reilly and her team from Memorial Sloan Kettering Cancer Center in New York hypothesized that Daraxone Lasib, which targets the K-Ras protein, could suppress the signaling that fosters cancer cell growth.

The research involved 500 patients suffering from metastatic pancreatic cancer across the United States, Europe, and Asia who had previously shown no response to initial chemotherapy. Participants were divided into two groups: one receiving daily Daraxone Lasib, while the other continued with standard chemotherapy infusions.

During the American Society of Clinical Oncology meeting on May 31, researchers revealed that those taking Daraxone Lasib experienced an average survival of 13.2 months, compared to 6.7 months for those undergoing traditional chemotherapy. “This is fantastic news,” Acedo remarked, emphasizing the treatment’s historical significance in enhancing survival outcomes for advanced pancreatic cancer patients.

Furthermore, only 1% of patients in the Daraxone Lasib group discontinued the drug due to side effects, such as mild rashes, in contrast to 11% of chemotherapy patients who stopped due to fatigue and other adverse effects. “The simplicity of taking a daily pill is a significant advantage over the invasive nature of chemotherapy, which requires frequent hospital visits,” Acedo concluded.

O’Reilly indicated that their findings have been submitted to the U.S. Food and Drug Administration (FDA), and they are optimistic about an approval for Daraxone Lasib for metastatic pancreatic cancer patients who have already received chemotherapy in the near future.

Nonetheless, Acedo warns, “While a few additional months of life would indeed be beneficial, we are still investigating the long-term outcomes.” Future studies may explore the potential advantages of combining Daraxone Lasib with other innovative therapies or chemotherapy regimens.

O’Reilly’s team is actively pursuing this line of research in ongoing clinical trials, as well as evaluating whether Daraxone Lasib could serve as an effective first-line treatment for previously untreated patients.

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Source: www.newscientist.com

Revolutionary Viral Injections Stop Pancreatic Cancer Progression in Three Patients

Posted on May 29, 2026 by Igor Mitreski

Scanning Electron Micrograph of Pancreatic Cancer Cells

Anne Weston, EM STP, Francis Crick Institute/Science Photo Library

Scanning electron micrograph of pancreatic cancer cells — Scanning Electron Micrograph of Pancreatic Cancer Cells

Anne Weston, EM STP, Francis Crick Institute/Science Photo Library

In a groundbreaking clinical trial in the United States, researchers have found that a novel viral treatment halted the progression of pancreatic cancer in three patients. While further assessments in larger trials are necessary, these early results are promising, particularly given that only minimal quantities of the virus were administered during initial safety tests.

According to Masato Yamamoto, who spearheaded the research at the University of Minnesota, “The efficacy exceeded our expectations, particularly considering we injected merely one-tenth of the targeted dose for pancreatic cancer.”

Pancreatic cancer is notoriously known as one of the deadliest cancers. This is due in part to the fact that symptoms often emerge late, when the cancer has typically advanced beyond the point of surgical removal. For patients diagnosed with this illness, the prognosis is grim: they usually survive for only about 3 to 6 months.

The stiffness of pancreatic tumors presents another significant challenge, inhibiting chemotherapy drugs from penetrating effectively. As Dr. Yamamoto aptly notes, “Pancreatic tumors are as hard as a hockey puck.” Additionally, these tumors can evade detection by the immune system, rendering immunotherapy treatments that boost immune activity against cancer cells largely ineffective.

One of the trial participants had a pancreatic tumor measuring 7 centimeters in diameter and underwent treatment about a year ago, with the other two patients treated subsequently. Fortunately, their tumors have not grown since treatment began. “They are all alive and exhibit clinically stable disease,” Dr. Yamamoto shared at the Annual Meeting of the American Society for Gene and Cell Therapy held earlier this month in Boston, Massachusetts. An additional 15 patients are now set to receive higher doses to determine the optimal treatment level.

Dr. Kai Brown, a pancreatic surgeon at the Royal North Shore Hospital in Sydney, cautioned, “While this shows intriguing early promise, we must maintain a cautious optimism. The history of oncology is riddled with initially encouraging signals that have vanished by the time rigorous phase III [late-stage] testing was completed. Thus, these initial results ought to be viewed as hypothesis-generating.” Notably, the trial currently lacks a control group, making it difficult to ascertain if the cancer-killing virus is more effective than existing treatments.

The virus being tested is a genetically modified adenovirus designed to proliferate specifically within tumors while avoiding healthy tissues. Its replication is activated by cyclooxygenase 2 (COX-2), an enzyme found in much higher levels in cancer cells than in normal cells. Upon infecting cancer cells, the virus can rupture and lead to their death, thereby releasing more virus to infect adjacent cancer cells.

During this trial, the virus was injected directly into the tumor via a thin tube guided down the patient’s throat, reaching the pancreas. An ultrasound probe at the tube’s end assisted in visualizing the tumor’s location.

Dr. Yamamoto speculated that the tumor’s growth has halted without regression likely due to the low treatment dosage. He believes that as the virus replicates, the number of infected tumor cells may diminish over time.

As tumor cells begin to break apart, the immune system may identify the cancer and initiate its attack. “The patient’s immune system may recognize that something is wrong and start targeting the tumor,” he explained. If successful, this treatment could potentially combat metastatic pancreatic cancer as well.

To enhance this innate immune response, Yamamoto and his team plan to combine viral therapies with immunotherapies, including checkpoint inhibitors—drugs that block proteins preventing the immune system from attacking cancer cells—in future clinical studies.

Historically, adenoviruses have caused cold and flu-like symptoms in their unmodified form, but they have shown promise as cancer treatments. In the 1950s, for example, women with cervical cancer were treated with unmodified adenovirus, witnessing some success in clinical trials. However, safety and efficacy issues highlighted the need for genetic engineering to tailor adenoviruses to specifically target cancer cells.

The only FDA-approved cancer-killing virus, T-VEC, is a genetically modified herpes simplex virus injected directly into melanoma tumors, inducing cell rupture and death.

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Source: www.newscientist.com

Enhancing CAR T Cell Therapy: The Impact of First Eradicating Cancer Cells

Posted on May 15, 2026 by Igor Mitreski

Illustation of CAR T cell therapy for melanoma, a form of skin cancer

Nemeth Laszlo/Shutterstock

Diagram illustrating CAR T cell therapy for melanoma treatment — Illustation of CAR T cell therapy for melanoma, a form of skin cancer

Nemeth Laszlo/Shutterstock

Innovative therapies are transforming the treatment landscape for blood and skin cancers, with recent studies highlighting enhanced effectiveness. In murine models with advanced skin cancer, researchers have discovered that manipulating the physical properties of cancer cells amplifies the efficacy of immunotherapy—specifically, CAR T-cell therapy. This promising breakthrough could significantly improve survival rates for patients undergoing immunotherapy.

“This groundbreaking concept addresses a critical medical issue from a physical perspective,” notes Lee Sui from Queen Mary University of London, who is not associated with this research. “The outlook is very hopeful.”

Cancer cells are often softer when compared to healthy cells, which poses challenges. T cells, vital components of the immune system responsible for targeting cancer, sense environmental stiffness.

“We examined whether the softness of cancer cells allows them to evade the immune response and how T cell mechanosensing affects the cellular response to cancer,” explains Lee Tan, who presented his findings on May 11 at an academic conference hosted by the Swiss Federal Institute of Technology in Lausanne, Switzerland. The Biophysical Immunoengineering: From Insights to Clinical Applications conference in London focused on these innovative approaches.

The researchers set out to uncover why cancer cells exhibit softness by contrasting their membranes with those of healthy cells. They discovered that both murine and human cancer cells tend to be softer due to high cholesterol content in their membranes.

The team subsequently injected 24 mice with melanoma cells, notorious for being the deadliest skin cancer. Nine days post-injection, the mice received genetically modified T cells specifically designed to target the tumor, emulating CAR T-cell therapy, which is approved for conditions like acute lymphoblastic leukemia and B-cell lymphoma.

Additionally, the mice underwent three injections over five days of IL-15, a protein that heightens the cancer-killing capacity of tumor-specific T cells.

Crucially, only half of the mice received a third treatment involving methyl beta-cyclodextrin (meβCD), a compound that reduces cholesterol levels in cell membranes, administered directly into the tumors daily from day 9 to day 18 post-cancer cell injection. The other mice received saline as a control.

After roughly one month, all 12 mice that did not receive meβCD succumbed to rapidly-growing tumors. In stark contrast, only seven mice in the meβCD group perished, while five experienced complete tumor resolution. “The results are compelling. Very encouraging,” states Lance Cam from Columbia University, New York.

Further analysis indicated that meβCD enhanced the adherence of tumor-specific T cells to tumor cells by stiffening them. Consequently, T cells were more effective in delivering toxic agents such as perforin, which perforates and obliterates cancer cells.

The research team aims to extend this approach to a broader array of tumors in mice, according to Tang. “The significant challenge lies in ensuring this understanding translates to human applications,” Kam emphasizes. Few successful immune-targeting drugs in mice yield equivalent results in humans, primarily due to immune system disparities. However, since cancer cells tend to be soft in both species, there is potential for therapies that modify cancer cell stiffness to be more effective.

Moreover, researchers are actively working on developing therapeutics with effects akin to meβCD that can be delivered with a single injection.

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Source: www.newscientist.com

Rare Case: Woman’s Cancer Goes into Remission Without Treatment

Posted on May 5, 2026 by Igor Mitreski

X-ray of a woman’s arm before biopsy: Arrow highlights the tumor

Gannon MC, Gabor RM, Gupta A, et al. (April 15, 2026)

A remarkable case involves a woman whose cancerous tumor on her arm is now in remission, attributed to a biopsy that triggered a powerful immune response. This unique scenario exemplifies how a biopsy can potentially change the fate of some cancer patients.

She is one of only nine known cases where a biopsy uncovered this specific type of cancer affecting connective tissue, which spontaneously resolved within weeks.

“It’s quite extraordinary,” says Toby Lawrence from the Marseille Lumigny Immunology Center, not directly involved in this case. “This suggests there was an immune activation in response to the biopsy injury, rapidly halting tumor growth.”

The 59-year-old woman noticed a rapidly enlarging lump, which reached two centimeters, before seeking medical attention. “The symptoms were escalating quickly and causing discomfort. She was understandably concerned,” states Rohit Sharma from Marshfield Clinic Health System in Wisconsin.

Sharma and his team marked the tumor’s location with tattoo ink and performed a thin-needle biopsy. They identified the growth as a myxofibrosarcoma, which contained highly malignant cells, posing a risk of metastasis. “Cancer often leads to fatal metastasis,” Sharma warns.

Two weeks later, the woman returned for tumor removal surgery, but astonishingly, the tumor had completely vanished. “She reported symptom relief within just three to four days post-biopsy,” says Sharma.

To confirm the disappearance of the tumor, the surgical team removed surrounding tissue, which showed no cancer cells. “The timing indicates that an immune response was activated,” Sharma explains. The phenomenon of cancer disappearing post-biopsy is extremely rare, typically observed in cancers that the immune system can easily identify, such as skin cancers.

A biopsy can destroy some cancer cells and release inflammatory signals that activate immune cells, like natural killer cells, which can eliminate damaged tumor tissue within days. This could trigger an even stronger immune response as T cells identify and attack remaining cancerous cells.

However, such an extraordinary immune reaction does not occur for most individuals. Factors like genetics and environmental triggers likely play a role in this rare phenomenon, according to Lawrence.

Magnetic Resonance Imaging Scan of the Tumor

Gannon MC, Gabor RM, Gupta A, et al. (April 15, 2026)

By analyzing the genomes and medical histories of these exceptional cases, researchers aim to uncover strategies that could enhance overall cancer treatment efficacy. Understanding the unique immune responses in mice with cancer resulting from minor tissue damage may hold the key to unraveling these mechanisms, suggests Caetano Reis e Souza at the Francis Crick Institute in London. “If we can learn how biopsies expose cancer cells to the immune system, it might pave the way for novel therapeutic drugs,” he posits.

Sharma’s research team is planning to explore this phenomenon further in the upcoming years by establishing a database of similar unique cancer cases.

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Source: www.newscientist.com

Rising Cancer Rates in Young People: Exploring the Unknown Causes

Posted on April 29, 2026 by Igor Mitreski

Colorectal cancer is on the rise, particularly among younger individuals.

Getty Images North America Copyright: Paul Morigi/Getty Images for Fight Colorectal Cancer

Colorectal Cancer Awareness — Colorectal cancer is on the rise, particularly among younger individuals.

Getty Images North America Copyright: Paul Morigi/Getty Images for Fight Colorectal Cancer

Research into the rising incidence of cancer among young individuals has generated more questions than definitive answers. While one study indicates that increasing obesity rates may account for a fraction of this trend, it doesn’t provide a comprehensive explanation.

According to Montserrat Garcia-Crosas from the Institute of Cancer Research (ICR) in London, the main takeaway is that although Body Mass Index (BMI) serves as a significant indicator, much of the increase remains unexplained.

Numerous global studies have documented a rise in cancer cases among adults under 50. Notably, the incidence of colorectal cancer has surged by about 50% in countries including the United States, Australia, and Canada since the 1990s.

To investigate the reasons behind this trend, Garcia-Crosas and colleagues analyzed cancer data in the UK alongside population trends related to risk factors such as obesity. Their findings indicated that 11 types of cancer are rising among individuals aged 20 to 49, with breast and colorectal cancers being the most prevalent. Other malignancies include liver, kidney, and pancreatic cancers, exhibiting growth rates between 1% and 6% annually.

The researchers discovered that the incidence of nine out of these 11 cancers was also increasing in individuals over 50, suggesting some common underlying factors. However, ovarian cancer and colorectal cancer were exceptions to this pattern, as noted by Garcia-Crosas.

The team also explored behavioral factors linked to these 11 cancers as identified by the International Agency for Research on Cancer, which include alcohol consumption, smoking, physical inactivity, body mass index, and dietary habits related to fiber and processed meats. “These researchers provide the strongest evidence connecting these factors,” Garcia-Crosas stated.

Despite the stable or improving nature of these risk factors over time, BMI remains a consistent concern, particularly given the rising rates of obesity. However, the link between obesity and the increase in cancer among young people is only partially understood. For instance, only about 20% of the rise in colorectal cancer among young women can be attributed to increasing BMI, as per Garcia-Crosas.

According to team member Mark Gunter at Imperial College London, extensive research is currently ongoing to identify the causes of this troubling trend. Potential factors being examined include a higher consumption of ultra-processed foods, substances known as PFAS (forever chemicals), and antibiotics affecting the gut microbiome.

Your analysis suggests that the increase in cancer cases among youths likely stems from a combination of elements rather than a single cause, and they could not exclude the possibility that diagnostic practices may also be influencing these statistics.

This rise should also be considered in context, as highlighted by Amy Berrington at ICR. In the UK, only about 3,000 bowel cancer cases are reported annually among individuals aged 20 to 49. Consequently, a 3% increase signifies approximately 100 more cases each year. “These trends are relative, and the overall increase in cases remains modest,” Berrington elaborated.

The study did not include cervical cancer due to the significant decrease in cases among women who received the HPV vaccine during childhood.

Looking ahead, Berrington draws attention to data through 2023, expressing optimism as the upward trend seems to be stabilizing. Furthermore, if obesity is a contributing factor to the rise in cancer diagnoses, emerging GLP-1 weight loss medications, such as semaglutide, may offer a potential solution. “Should obesity rates decline due to the adoption of these medications, we could witness a reduction in some obesity-related cancers in the future,” Professor Gunter concluded.

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Source: www.newscientist.com

Does Catching a Cold Slow Lung Cancer Metastasis?

Posted on April 23, 2026 by Igor Mitreski

The lungs as a common site for cancer metastasis

Cavallini James/BSIP/Universal Images Group/Getty Images

The lungs and cancer — The lungs as a common site for cancer metastasis

Cavallini James/BSIP/Universal Images Group/Getty Images

Studies indicate that respiratory infections may temporarily inhibit the spread of cancer to the lungs
from other body parts. Recent experiments involving the respiratory syncytial virus (RSV)—known for causing cold-like symptoms and infecting nearly all children by age two—demonstrated its ability to hinder breast cancer cell colonization in the lungs. This suggests that the activation of infection-fighting proteins during such infections might be leveraged for therapeutic purposes.

According to research, the majority of cancer fatalities result from the metastasis of tumor cells from their original locations. Although early-stage cancer can often be treated effectively through surgery or radiation, once it metastasizes, treatment challenges increase significantly, with low success rates. As highlighted by David Withers from the University of Oxford, this presents a major clinical hurdle.

The implications of respiratory infections, including influenza and COVID-19, on cancer metastasis are captivating researchers, especially given the lungs’ susceptibility as a common site for such spread.

In mouse studies, RSV successfully triggered an immune response that inhibited the migration of breast cancer cells to the lungs. Cecilia Johansson from Imperial College London remarked, “This finding is remarkable, as it represents a novel aspect of viral impact on cancer.”

The research team infected 23 mice with RSV, while 16 healthy mice were used as controls. Following a 24-hour period, all mice received injections of breast cancer cells. After 28 days, lung tumor nodules in the RSV-infected mice were reduced by 65 to 70 percent compared to controls.

However, the size of the nodules that formed remained similar in both groups, indicating that the virus did not significantly impede cancer cell proliferation once they were established in the lungs. This aligns with previous studies showing that the viruses associated with swine flu and COVID-19 could activate dormant cancer cells after they have metastasized to the lungs.

Johansson and her team subsequently explored the role of type I interferon, a protein within lung cells that inhibits viral replication. Their findings revealed that this protein makes it considerably more challenging for cancer cells to develop new tumors.

To determine whether administering type I interferon could replicate the effects of RSV, researchers provided another group of mice with interventions, receiving doses of interferon prior to cancer cell injection. Initial results suggested that interferon was “slightly” more effective than the viral infection at limiting tumor cell ingress into the lungs.

“The study indicates that the type I interferon response, typical of acute viral infections, induces significant alterations in the lung epithelium,” explained Withers. “Although still in the preclinical phase, these results uncover exciting avenues to potentially enhance patient protection against metastasis.”

Researchers speculate that multiple mechanisms contribute to how type I interferon prevents tumor cell dissemination. Their focus remained on one particularly impactful method involving galectin-9, a protein produced in response to these interferons.

Johansson is optimistic that these findings could eventually lead to new drugs designed to thwart the spread of breast cancer and other tumors to the lungs. She stated, “Despite being early preclinical findings, we can test these strategies to develop new treatments against cancer without relying on viral infections.”
Claire Bennett from University College London did not participate in the study.

While the theoretical approach posits that the same strategy could thwart cancer spread to the lungs from various body sites, Johansson underlines the need for further investigation. She emphasizes that delivering type I interferon intranasally may create harmful airway inflammation.

The research team aims to conduct additional studies to deepen the understanding of interferons’ effects on cancer propagation. “We aspire to explore whether we can emulate this effect using IFN-inducing agents and how to effectively target the lung epithelium and stroma,” Johansson concluded. “Our goal is to eventually translate these findings into human studies and identify therapeutic targets in clinical settings, though that lies ahead.”

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Source: www.newscientist.com

Create an Extensive Cancer Data Library: A Comprehensive Guide – Sciworthy

Posted on April 17, 2026 by Igor Mitreski

Computational cancer researchers utilizing machine learning technology face a critical challenge. Large datasets are available for training machine learning models, but the process is demanding due to inconsistencies in data formats, names, structures, and other attributes. Consequently, when scientists analyze different cancer types or apply varying data cleaning methods, the performance of the resulting models can diverge significantly.

This discrepancy has created a gap between available datasets and their practical usability, posing a significant barrier for researchers lacking specialized bioinformatics training. Variations in data processing methodologies further complicate the comparison of different machine learning approaches, making it challenging to identify the optimal method for tasks such as classifying patient samples as benign or malignant.

In response, collaborative researchers from Japan and the United States have developed a robust database tailored for machine learning applications, comprising genetic and molecular data from over 8,000 cancer patients. They named this groundbreaking database MLOmics. Similar to a well-organized library, MLOmics provides cancer data ready for immediate use by computer models, eliminating the need for extensive data preprocessing.

To create MLomics, researchers retrieved patient samples from 32 cancer types from publicly accessible databases, including the Cancer Genome Atlas. They collected four distinct types of molecular data per patient, comprising two DNA product types. The dataset includes transcriptomics data, data on DNA regions termed copy number variation, and details regarding chemical DNA markers known as methylation. For transcriptomics data, the team labeled experimental factors influencing data quality, eliminated contamination from non-human samples, and addressed unlabeled values.

For copy number variation data, researchers focused on cancer-specific repeated sequences, identifying and labeling recurrent aberrant repeats along with their corresponding genes. They adjusted methylation data to eliminate biases caused by various experimental platforms. In addition, a uniform identifier was assigned to all molecular data to standardize naming conventions.

Subsequently, the team developed a coding pipeline to assess data quality and integrate each patient’s molecular data types into a single, cohesive dataset using the multi-omics approach, which amalgamates diverse molecular measurements. They matched each patient sample with its associated cancer type, thereby creating an organized dataset prime for analysis.

The researchers designed 20 task-aware datasets across three categories of machine learning problems, establishing appropriate metrics for model evaluation in each category. They aimed to showcase how MLOmics can be employed for a variety of common research tasks.

The first category is classification, comprising six datasets that facilitate training models to categorize samples into known classes, such as malignant or benign tumors. The second category, clustering, includes nine datasets that allow scientists to explore how samples group naturally based on molecular characteristics when predefined labels are absent. The final category, data completion, consists of five datasets aimed at addressing incomplete molecular data caused by technical or experimental errors, detailing how models can estimate or fill in missing values, a common challenge in real-world scenarios.

The researchers also organized the MLOmics database into three distinct sections, each with comprehensive usage guidelines. The first section primarily offers task-aware cancer multi-omics datasets formatted as comma-separated values (CSV files). CSV files were selected for their efficiency with large genomic datasets, as they are easily processed by programming languages like Python and R. The second section provides code files designed to assist scientists in model development and evaluation. Finally, the last section includes links to additional resources that complement the primary datasets, ensuring accessibility for all interested researchers, regardless of their background.

In conclusion, the researchers affirmed that MLOmics represents a significant asset for the cancer research community, allowing scientists to concentrate on enhancing algorithms instead of expending time on data preparation. They highlighted MLOmics’ suitability for non-specialists, encouraging interdisciplinary research and broader biological studies. The team is committed to continuously updating MLOmics with new resources and tasks in alignment with advancements in the field.

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Source: sciworthy.com

Creating a Comprehensive Cancer Data Library: A Step-by-Step Guide by Sciworthy

Posted on April 9, 2026 by Igor Mitreski

Computational cancer researchers leverage machine learning technology to tackle a significant challenge: the vast amounts of data available for training machine learning models. Despite this abundance, training is hindered by inconsistent data formats, structures, and properties. Consequently, when scientists apply various cancer types and data cleaning procedures, the resulting models can yield vastly different outcomes.

Researchers have identified the disparity between available and usable datasets as a considerable obstacle for scientists lacking specialized bioinformatics training. Furthermore, varied processing strategies make it difficult to equitably compare new machine learning techniques and identify the most effective method for specific cancer research tasks—such as classifying patient samples into benign or malignant categories.

To address this issue, a collaboration between researchers in Japan and the United States has resulted in the development of a comprehensive database tailored for machine learning applications. This database, named MLOmics, encompasses genetic and molecular information from over 8,000 cancer patients. Similar to a well-organized library, MLOmics offers cancer data that can be directly utilized by computer models, eliminating the need for extensive preprocessing.

In constructing MLOmics, the team gathered patient samples from 32 cancer types sourced from publicly available databases like the Cancer Genome Atlas. Data collection included four distinct types of molecular information, consisting of two forms of DNA products: Transcriptomics data, data on repetitive DNA regions termed Copy Number Variations, and information about chemical DNA tags known as Methylation. The team meticulously labeled experimental sources affecting data quality, eliminated contamination from non-human samples, and removed unlabeled values specific to transcriptomics data.

For the copy number variation data, researchers focused on cancer-specific repeats, identifying and labeling recurrent aberrant repeats along with corresponding genes in those regions. They also adjusted the methylation data to eliminate biases from various experimental platforms. Each processed molecular data type was then assigned a standardized identifier to mitigate discrepancies in naming conventions.

Subsequently, a coding pipeline was established to assess data quality and consolidate each patient’s molecular data types into a unified dataset—an approach known as multi-omics, as it integrates various molecular measurements. The researchers matched each patient’s sample to its relevant cancer type, resulting in an organized dataset suitable for analysis.

The research team developed 20 task-aware datasets across three categories of machine learning problems, providing crucial metrics for model evaluation in each. Their objective was to showcase how other scientists can effectively utilize MLOmics for a range of common tasks.

The first category focuses on classification, including six datasets that assist scientists in training models to categorize samples as malignant or benign. The second category, clustering, incorporates nine datasets that reveal natural groupings among samples based on molecular patterns when predefined labels are absent. The final category, data completion, features five datasets aimed at addressing incomplete molecular data resulting from experimental or technical challenges, showcasing how models estimate or fill in missing values—a common occurrence in real-world scenarios.

The MLomics database is organized into three sections, each offering detailed usage guidelines. The first section includes task-aware cancer multi-omics datasets in comma-separated values (CSV) format. This format is ideal for large genomic datasets, as programming languages like Python and R have built-in functions for effective reading, writing, and analysis. The second section offers code files to facilitate model development and application of evaluation metrics, while the final section contains links to supplementary resources to enhance biological analyses and ensure the database is accessible to all researchers, regardless of their educational background.

In conclusion, the researchers assert that MLOmics represents a vital resource for the cancer research community, enabling researchers to concentrate on developing superior algorithms instead of data preparation. They highlight the accessibility of MLOmics for non-specialists and its support for interdisciplinary and broader biological research. The team is committed to continuously updating MLOmics with new resources and tasks to align with advancements in the field.

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Source: sciworthy.com

Alarming Factors Behind the Rise of Colorectal Cancer in Individuals Under 50

Posted on March 20, 2026 by Igor Mitreski

Tragic news from Dawson’s Creek star James Van Der Beek, who recently succumbed to bowel cancer at just 48 years old, has brought attention to the alarming surge of early-onset cancer cases.

New research highlighted in Lancet Oncology indicates that the incidence of this disease among individuals under 50 has escalated in 27 out of 50 countries over the last decade—an increase that cannot be simply attributed to genetic factors.

“That’s very concerning,” states Dr. Trevor Rowley, a researcher at the Wellcome Sanger Institute. “While we have hypotheses we are examining, the need for additional data remains critical.”

It is yet unclear if a single factor is responsible for this rise or if a combination of elements is at play, but these are currently the leading theories.

Obesity and Early-Onset Cancer

Adolescent obesity is among the recognized risk factors for early-onset colorectal cancer, along with conditions like type 2 diabetes and metabolic syndrome that can further heighten this risk. Onset of disease is increasingly attributed to these health issues.

“Obesity is a well-known risk factor for colorectal cancer across all age demographics,” asserts Dr. Peter Campbell, professor of epidemiology at Albert Einstein College of Medicine.

“Excess body fat leads to chronic inflammation and metabolic changes, which include elevated insulin levels and growth factor signaling—conditions that can foster the development of precancerous polyps and cancers in the colorectum.”

Excess body fat can trigger inflammation and hormonal changes, heightening your risk of colon cancer – Photo credit: Getty

However, Campbell notes that while the number of individuals under 50 who are overweight or obese is rising, this alone does not fully account for the increase in bowel cancer cases. One analysis revealed that obesity was a contributing factor in only about 13% of early-onset colorectal cancer cases.

Thus, other significant risk factors likely play a role, some of which manifest surprisingly early in life.

The Role of Intestinal Bacteria

Cancer does not develop overnight. The progression from initial DNA damage to tumor formation can take years or even decades. To unravel the origins of colorectal cancer, especially in young adults, Rowley and his team are investigating the microbiomes of infants.

The leading theory posits that a toxic enzyme known as colibactin may be a key contributor to early-onset colorectal cancer.

This enzyme is known to cause unique patterns of DNA damage in colon cells that are notoriously difficult to repair. A study published in Nature found that colibactin-related DNA mutations were 3.3 times more frequent among colorectal cancer patients under 40 compared to those over 70.

Certain gut bacteria produce toxins that can damage DNA in the colon, increasing cancer risk decades later – Photo credit: Getty

Numerous gut bacteria species are known to produce colibactin, including Escherichia coli, Klebsiella pneumoniae, and Citrobacter coseri.

It’s believed that some individuals acquire these pathogens in early life, setting the stage for future DNA damage and increased cancer susceptibility decades later.

“My lab has amassed a significant database of baby microbiomes from around the globe. For instance, about 25% of infants born in the UK have colibactin in their gut microbiome,” Rowley shares.

Read more:

The prevailing hypothesis is that more infants are acquiring pathogenic enteric bacteria in their colons compared to earlier generations. But why?

Some researchers point to the rising use of antibiotics in early childhood. These medications can unintentionally decimate significant portions of the beneficial gut microbiome, facilitating invasion by harmful bacteria.

Others speculate that increased C-section births, reliance on formula feeding, or other factors may be contributing to this trend. “These are all avenues we’re researching,” Rowley notes.

Ultra-Processed Foods

Complicating the situation is the fact that many people may carry colibactin DNA mutations without ever developing cancer.

This phenomenon could be attributed to their immune systems effectively identifying and eliminating malignant cells before tumor formation occurs. “While a mutation is necessary for cancer development, the immune system also plays a crucial role,” Rowley explains.

Consequently, another theory suggests that diets high in ultra-processed foods (UPF) may influence the development of colorectal cancer. A study published in Nutrition in 2021 indicated that regular intake of UPF may lead to immune system dysfunction.

Researchers suggest that a diet high in ultra-processed foods may promote abnormal growth in the intestines, leading to cancer – Photo courtesy of Getty

UPF may also encourage the growth of pro-inflammatory intestinal bacteria such as Fusobacterium nucleatum, which is believed to increase risk by enabling tumors to evade immune system surveillance.

Last year, a study conducted by researchers at Harvard Medical School, published in JAMA Oncology, found that women consuming up to 10 servings of UPF per day had a 45% higher risk of developing intestinal polyps compared to those who ingested just three servings daily. “Such polyps can precede colorectal cancer,” Campbell warns.

Environmental Toxins

While the three theories mentioned above have substantial backing, researchers continue to explore fresh hypotheses, including the potential impact of environmental toxins like microplastics and nanoplastics.

A study published last October recreated a gut microbiome model using stool samples from healthy participants, who were subsequently exposed to five common microplastics.

The findings suggested that particular plastic particles could alter microbiome composition.

Frank Frizell, a Professor of Colorectal Surgery at the University of Otago, speculates that plastic accumulation in the intestines may be linked to the rise of colorectal cancer among the youth.

“It’s plausible that they could penetrate the protective mucus layer of the intestinal lining, akin to poking a pinhole in a water balloon,” Frizell explains. “The plastics likely aren’t toxic in themselves, but they may act as vectors for harmful bacteria and chemicals or disrupt the mucus barrier.”

Potential Solutions

Ultimately, while many unknowns remain, further understanding of the causes behind early-onset colorectal cancer could pave the way for new solutions.

One avenue worth exploring is phage therapy, which involves introducing viruses into the intestine that target colibactin-producing bacteria, effectively halting toxin production. Another possibility is the development of probiotics designed to enhance the growth of beneficial gut bacteria, thereby counteracting harmful pathogens.

Phage therapy employs targeted bacteriophages to eliminate specific bacteria, with some firms aiming to utilize this approach to combat colibactin, a toxic enzyme known for causing DNA damage. – Photo courtesy of Science Photo Library

“Certain companies are exploring the use of phages to eliminate bacterial strains that produce colibactin,” Rowley notes.

“We’re leveraging a database of early childhood microbiomes to identify beneficial species and strains that could invade and prosper in babies with less diverse microbiomes during their initial months of life.”

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Source: www.sciencefocus.com

Understanding Machine Learning in Breast Cancer Prediction – Sciworthy

Posted on March 12, 2026 by Igor Mitreski

Cells utilize their internal DNA to produce essential products, such as proteins, through a process termed gene expression. However, scientists and health organizations have identified that gene expression datasets often suffer from inadequate patient samples and excess genes per sample, creating significant challenges in the global fight against cancer. This discrepancy hinders the ability to identify and prioritize critical changes in gene expression that differentiate cancer cells from healthy ones, a phenomenon referred to as the curse of dimensionality.

While machine learning techniques can analyze existing patterns within these expansive datasets to classify samples as cancerous or non-cancerous, this presents additional hurdles. Clinicians are often skeptical of machine learning conclusions due to a lack of understanding regarding model decision-making processes, leading to what is known as the black box problem. Consequently, researchers are striving to develop methodologies that clarify how these models derive their predictions.

A collaborative research team across multiple institutions in Africa concentrated on explicating breast cancer model predictions. They accessed publicly available gene expression data from a global database known as The Cancer Genome Atlas, which compiles data on approximately 20,000 genes from 1,208 breast cancer samples. Their primary objective was to isolate a select few genes from those 20,000 that could reliably predict cancer presence in tissue samples.

Initially, the researchers refined their dataset to 3,602 genes that exhibited differential expression between breast cancer and healthy cells. They then implemented an algorithm to experiment with various gene combinations, aiming to identify the smallest set of genes that consistently yielded promising results. This process is analogous to conducting thousands of mini-races with different runners to determine which runner consistently finishes first, despite all ultimately reaching the finish line.

Subsequently, they utilized diverse machine learning techniques to train and optimize several models based on the expression data of the genes chosen by the algorithm. Remarkably, all models demonstrated high accuracy, predicting cancer status with at least 98% reliability. The next questions arose: “Which genes contribute to model efficacy?” and “How do these genes influence predictions?”

The team employed four distinct statistical interpretation methods known as feature importance techniques to pinpoint the genes most critical to model performance. The first method illustrated how each model’s predictions shifted based on gene expression levels. The second showcased the interplay between multiple genes informing model decisions. The third quantified the overall impact of each gene on the model’s judgement, facilitating a ranked analysis, while the final method evaluated how accurately a single gene could predict breast cancer independently.

Through their analysis, the researchers identified seven genes consistently represented across all trained models and feature importance evaluations. They verified that these genes are associated with biological functions influencing cancer progression, such as tissue repair, regulation of cellular substance transport, and immune response management.

While different models generally agreed on key genes, variations in their exact rankings and influence scores were noted. The researchers explained that biological data is often complex, leading models to interpret various aspects of the same data, suggesting that integrating insights from multiple machine learning models yields superior outcomes compared to depending on a singular model.

The team acknowledged several challenges. The gene selection algorithm required nearly six hours on a high-performance laptop, which may not be practical for larger datasets. They also recognized the potential omission of crucial genes during the selection process. Additionally, despite the extensive dataset, it may not encapsulate the full diversity of breast cancer globally, potentially limiting the model’s applicability across different populations. The researchers concluded that merging machine learning approaches with clear and interpretable methods marks the future of cancer prediction, fostering clinical trust in machine learning-driven insights.

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Source: sciworthy.com

Detecting Cancer Cells in Complex Tissue Mixtures: Insights from Sciworthy

Posted on February 21, 2026 by Igor Mitreski

Cancer disrupts multiple layers of the biological blueprint, including the order of DNA sequences and the chemical markers on DNA known as DNA methylation. In cancer patients, tumor samples obtained from areas like the colon or skin contain a blend of healthy cells, which exhibit normal levels of methylation, alongside cancer cells that show abnormal methylation patterns. This mixture complicates doctors’ efforts to differentiate between the two and identify which methylation signals are genuinely sourced from the tumor.

Moreover, harvesting tumors directly often necessitates painful surgical procedures. Some scientists propose using blood samples as an alternative for initial diagnosis. However, blood samples generally face the same challenge, frequently containing only minute traces of cancer DNA.

Traditionally, scientists have averaged the methylation levels of numerous DNA fragments from patient samples to estimate the proportions of cancerous and normal DNA present. Unfortunately, this conventional approach overlooks valuable insights regarding rare and subtle disruptions to DNA. Researchers in Germany and Belgium contend that this missing information is vital for the early detection and diagnosis of cancer. Consequently, they have introduced a new analytical tool named Methylvert to tackle this issue. This tool examines individual DNA sequences to analyze DNA methylation, ensuring these subtle details are preserved.

The team developed MmethylBERT, utilizing the same technology that powers modern language models, such as ChatGPT, with a transformer architecture. They re-engineered this technology to interpret the language of DNA and its methylation signals rather than human language. Each DNA sequence served as a concise “sentence” for the model to analyze and discern the differences between tumor and normal DNA.

The researchers trained MmethylBERT in two phases. Initially, they exposed it to a template dataset derived from the human reference genome. This dataset was used to help the model recognize patterns in DNA sequences, independent of methylation or disease information. This step is akin to teaching students to read using only the letters that form words, without additional context. The model became adept at distinguishing various three-letter DNA combinations, recognizing that certain bases, particularly C and G in ATCG, manifest in specific patterns. The pre-training step proved crucial; omitting it would prevent the model from accurately classifying cancer cells versus normal cells.

In the second phase, they fine-tuned the pre-trained model using DNA sequences from actual cancerous and healthy samples, teaching the model to identify known tumor-specific methylation patterns. This strategy parallels instructing students on grammar, which adds context and meaning to words. The model learned that certain DNA regions exhibit high methylation levels in tumors and low or negligible methylation in normal cells, or vice versa. They devised a system that generates a probability score, indicating how likely each DNA fragment originates from tumor or normal tissue.

The team evaluated MmethylBERT against existing methods by employing simulated DNA sequence data of varying complexity. Their findings demonstrated that their method accurately detects cancer DNA, even while analyzing DNA fragments at genomic locations with minimal sequence reads—where traditional methods often falter. They successfully identified very small quantities of tumor DNA in the blood of colorectal and pancreatic cancer patients, further validating its applicability in non-invasive cancer detection.

Scientists noted that training models on human genome data is time-consuming, so they assessed whether a model trained on the mouse genome could analyze human cancer samples. Remarkably, the mouse-trained model performed nearly as well as the human-trained model when applied to human cancer data, resulting in only minor differences in the probability distribution. The researchers attributed this efficacy to the consistent organization of DNA across mammals, enabling models to transfer knowledge from one organism to another.

The researchers concluded that MethylBERT can identify cancer DNA in sequence data obtained from any sequencing platform, irrespective of the complexity of the methylation signal or the size of the tumor DNA in the sample. They also cautioned that the current version requires substantial computational resources for training and operation and have already commenced development on a more efficient iteration.

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FDA Fast-tracks First Inhalable Gene Therapy for Cancer Treatment

Posted on February 20, 2026 by Igor Mitreski

Innovative Gene Therapy Delivered as a Mist for Lung Cancer Treatment

Nico De Pasquale Photography/Getty Images

Inhaled Gene Therapy for Lung Cancer — Innovative Gene Therapy Delivered as a Mist for Lung Cancer Treatment

Nico De Pasquale Photography/Getty Images

An innovative inhaled gene therapy targeting lung cancer is rapidly advancing toward potential approval following encouraging results from clinical trials.

Dr. Wen Wee Ma at the Cleveland Clinic highlighted the findings at a recent American Society of Clinical Oncology conference in Chicago, stating, “Very encouragingly, this proves our hypothesis that the lung tumor actually shrunk.”

This groundbreaking treatment employs a virus to introduce immune-boosting genes into lung cells, enhancing their natural ability to combat tumors. Unlike traditional gene therapies, which often replace defective genes, this method focuses on modifying existing lung cells.

The unique inhalation delivery method represents a significant advancement in cancer treatment. “This is a completely different approach to anti-cancer treatment,” said Ma. Directly targeting the lungs enhances the efficiency and effectiveness of the treatment, particularly since lung cancer is notoriously difficult to treat with standard oral or intravenous therapies.

The therapy utilizes a harmless, modified herpes virus to inject two critical genes into lung cells: interleukin-2 and interleukin-12. These proteins, naturally produced by the body, help inhibit tumor growth. Unfortunately, tumors often diminish their effectiveness, necessitating the need for gene therapy to restore their production.

Since 2024, clinical trials have been ongoing with patients suffering from advanced lung cancer who have exhausted all other treatment options. The therapy is administered via a fine mist inhaled directly into the lungs.

At the oncology conference, Ma reported that the gene therapy has successfully reduced lung tumor sizes in three out of eleven trial participants, while also halting growth in another five. Although some patients reported side effects, such as chills and vomiting, no severe safety issues were noted.

Based on these promising outcomes, the U.S. Food and Drug Administration recently granted “Regenerative Medicine Advanced Therapy Designation” to the gene therapy, facilitating expedited approval processes for patient access.

However, it is important to note that this gene therapy is specifically designed for lung tumors and does not address tumors that have metastasized to other body parts. To expand its efficacy, Ma and his team are exploring combinations with immunotherapy and chemotherapy in a trial involving approximately 250 patients.

Crystal Biotech, the developer of this gene therapy, previously introduced the first FDA-approved gene therapy targeting the skin, using a similar modified herpes virus to treat patients with recessive dystrophic epidermolysis bullosa, a rare skin condition. The company is also developing inhaled gene therapies for cystic fibrosis and alpha-1 antitrypsin deficiency, both inherited lung diseases.

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Source: www.newscientist.com

Finding Hope Through the Lens: How Photography Transformed a Teenager’s Cancer Journey

Posted on February 3, 2026 by Igor Mitreski

In 2016, LJ was just 19 years old and on the brink of a transformative journey. After graduating from college with commendable grades, he was excited to explore the world. However, he soon discovered what seemed like a harmless lump on his neck.

“I remember finding a large lump on my neck,” he recalls. “I felt exhausted all the time. It started to interfere with my life.”

Despite visiting the doctor, LJ was convinced it was “just an infection” and delayed follow-up appointments until he was urgently called back for test results. “The doctor told me, ‘This is leukemia,’” LJ reflects. “I couldn’t believe it—cancer at my age? I didn’t even know what leukemia was back then.”

We spoke with LJ about his inspiring cancer journey, how photography became a vital coping tool during a year of intensive treatment, and how Macmillan Cancer Support played a crucial role in guiding him through pivotal decisions in his life.

LJ’s Story: A Life-Altering Diagnosis

In 2016, LJ received a diagnosis of acute lymphoblastic lymphoma, an aggressive cancer necessitating immediate action. Instead of diving into student life, he faced grueling hospital stays with a bleak prognosis of only a 5% survival rate.

“I was stuck in a hospital bed undergoing chemotherapy, surgeries, radiation therapy, and stem cell transplants… it was overwhelming,” LJ shares. “I endured numerous procedures and constant needles…”

“The hardest part is hearing that treatments aren’t effective,” he continues. “Chemotherapy fails, radiotherapy fails, surgery fails. There’s a lot of chaos and distress. Despite your hopes and beliefs, things might not go as planned.”

LJ and his tutor Margot: discovering a passion for photography during treatment

Finding Freedom in Photography

Before his diagnosis, LJ was a typical teenager, exploring creativity, traveling, skateboarding, and enjoying time with friends in London. Suddenly, he found himself “isolated in a room or a ward”, painfully aware that days felt like they had no end.

As the walls of his physical environment closed in, LJ discovered that photography and videography opened a new world for him. By documenting his experiences through photos and videos, he created a much-needed escape: a creative outlet and a way to process his reality.

“I had a little Canon PowerShot G7 camera at the time,” he shares. “Taking photos helped me express my feelings without leaving the hospital. I could capture my emotions and enjoy the creative process. It was incredibly fulfilling.”

Macmillan’s guidance empowered LJ to make important decisions during critical moments

Macmillan Support During a Crucial Time

During this challenging treatment phase, LJ came across vital information from Macmillan Cancer Support in the form of a pamphlet, which provided essential guidance for his future. “I received a leaflet from Macmillan about cancer and fertility,” he states.

“After multiple surgeries, fertility can be affected, and I learned that I might not be able to have children,” he reveals. “The insights in that pamphlet helped me comprehend my situation significantly.”

Now, a decade after his diagnosis and in remission, the support from Macmillan has made a lasting impact on LJ’s life. “Without that booklet, I would have likely made decisions I’d regret,” he states.

Gifts in wills fund over a third of Macmillan’s services, including the resources that aided LJ, ensuring continued access to trusted cancer support, from helplines to informational booklets and community support across the UK. Having clear guidance and support from Macmillan was pivotal for LJ in making informed decisions about sperm storage at a critical time.

Thanks to Macmillan’s support, LJ is dedicated to raising awareness about cancer in young men

Why Consider Leaving a Gift to Macmillan Cancer Support in Your Will?

As LJ approaches a decade since his diagnosis, he has transformed his life, establishing himself as a skilled fashion and event photographer. You can view his remarkable portfolio here. Additionally, he is involved with Macmillan, helping to spread cancer awareness among young men.

“Macmillan helped me share my story and be heard. If my experience inspires someone to keep fighting, then I feel fulfilled,” he adds.

In the UK, someone is diagnosed with cancer every 90 seconds. LJ understands the importance of having Macmillan’s support when it matters most, and he has a special message for those contemplating leaving a legacy gift.

“Each day, many people receive a cancer diagnosis. While no one can fully understand your feelings, having someone who can clarify information about your cancer is invaluable. That’s the kind of support Macmillan offers.”

Thanks to Macmillan’s guidance, LJ was able to better understand his situation while focusing on his passions. Your legacy gift will empower Macmillan to provide essential care to more individuals facing cancer, regardless of their background. For more information on how to leave a gift in your Will to Macmillan Cancer Support, request our free Gifting in a Will guide.

© Macmillan Cancer Support, a charity registered in England and Wales (261017), Scotland (SC039907) and the Isle of Man (604). Also active in Northern Ireland. A company by guarantee registered in England and Wales (company number 2400969). Isle of Man company number 4694F. Registered office: 3rd Floor, Bronze Building, The Forge, 105 Sumner Street, London, SE1 9HZ. VAT number: 668265007

Source: www.sciencefocus.com

How Early Cancer Treatment Before 3 PM Can Increase Patient Survival Rates

Posted on February 2, 2026 by Igor Mitreski

Timing Cancer Treatment: A Simple Yet Effective Intervention

Kenneth K. Lam/ZUMA Press/Alamy

The first randomized controlled trial investigating the timing of cancer immunotherapy has revealed that administering treatment earlier in the day may significantly enhance patient survival rates.

Human cells and tissues operate on a 24-hour cycle, known as the circadian rhythm, influencing various bodily functions including mood, metabolism, and immune response.

Numerous observational studies have indicated that cancer patients receiving checkpoint inhibitors (a class of immunotherapy drugs that empower the immune system to combat cancer) earlier in the day show a lower risk of disease progression and mortality.

Recently, Francis Levy and his team at the University of Paris-Saclay, France, conducted the first randomized controlled trial focused on chronotherapy—timing treatments based on circadian rhythms—utilizing both chemotherapy and immunotherapy.

In this study, 210 patients diagnosed with non-small cell lung cancer were given four doses of either pembrolizumab or sintilimab, two checkpoint inhibitors that function similarly.

Every three weeks, half of the participants received their doses before 3 p.m., while the others received treatments later. All patients also received chemotherapy immediately after each immunotherapy session. Chemotherapy targets rapidly dividing cells and is believed to have a lesser connection to circadian rhythms than immunotherapy.

This timing was strictly adhered to during the initial four cycles of the combined immunochemotherapy treatments. Following this period, all participants continued receiving the same medications until their tumors advanced or no longer responded, but without specific timing guidelines. Previous research suggests that the first four cycles are crucial, as noted by team member Zhang Yongchang from Central South University, China.

Participants were monitored for an average of 29 months post-initial treatment. Results showed that those treated before 3 p.m. had a median survival of 28 months, compared to 17 months for those treated later in the day. “The results are dramatically positive,” Levy stated. “Survival time nearly doubles.”

“When we compare our findings to significant trials that resulted in new drug approvals, such large effects are rarely observed,” noted Pasquale Innominato from the University of Warwick, UK. He emphasized that the study demonstrates a definitive link between treatment timing and survival outcomes, deeming it solid evidence of causation.

This dramatic improvement may be attributed to T cells, a type of immune cell targeted by checkpoint inhibitors, which tend to accumulate near tumors in the morning and gradually enter the bloodstream later. Administering immunotherapy earlier could position T cells closer to tumors, enabling more effective destruction, according to Levy.

Levy also emphasized the need for further studies to explore if more precise timing, such as 11 a.m., offers additional advantages compared to broader scheduled treatments. Innominato pointed out that having flexibility in timing is advantageous for busy healthcare facilities.

Further investigation is necessary to determine whether managing the timing of chemoimmunotherapy beyond the first four cycles yields greater benefits, Levy mentioned. Individual variability could also play a critical role; for example, a morning person may have different immune responses compared to a night owl.

Whether these findings apply to various cancer types remains an open question. Innominato anticipates similar results in other tumors commonly treated with immunotherapy, like skin or bladder cancers, but tempered his expectations for tumors such as prostate or pancreatic cancers that often resist treatments.

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Source: www.newscientist.com

AI-Enhanced Mammograms Lower Risk of Malignant Breast Cancer

Posted on January 30, 2026 by Igor Mitreski

AI Simplifies Cancer Detection in Mammograms

AMELIE-BENOIST/BSIP/Universal Images Group via Getty

Radiology Center — AI Simplifies Cancer Detection in Mammograms

AMELIE-BENOIST/BSIP/Universal Images Group via Getty

Recent studies indicate that women screened for breast cancer with AI-assisted radiology experience a significant reduction in the development of advanced cancer by their next screening compared to those assessed by a traditional radiologist alone, sparking hopes that AI technology could enhance patient outcomes.

“This is the first randomized controlled trial examining AI’s effectiveness in mammography screening,” states Christina Lång from Lund University, Sweden.

The AI-assisted method utilizes advanced software trained on over 200,000 mammography scans from 10 countries to evaluate the likelihood of cancer on a 1 to 10 scale based on distinctive visual patterns in the scans. Scans rated 1 to 9 are reviewed by a single experienced radiologist, while those with a score of 10, indicating a high likelihood of cancer, are assessed by two radiologists for a more thorough evaluation.

Previous research has shown that the AI approach can identify 29% more cancers compared to standard evaluations, where two radiologists review each mammogram without increasing the false-positive rates. “That’s truly impressive,” notes Fiona Gilbert, a doctor at Cambridge University who was not involved in the study.

Furthermore, Lång and her team have discovered that the AI approach significantly lowers the incidence of interval cancers—tumors that develop rapidly between regular screenings, making them particularly aggressive and prone to metastasis.

The study involved over 100,000 Swedish women aged 55 and older, with roughly half receiving standard breast cancer screening reviewed by two radiologists, while the other half were screened using an AI model developed by ScreenPoint Medical, with results evaluated by an experienced radiologist in Nijmegen, Netherlands.

Women who benefited from AI-assisted screening were, on average, 12% less likely to develop interval cancers compared to their counterparts undergoing standard screening. “We were thrilled when the results arrived,” Lang stated.

This improved outcome could be attributed to AI’s superior ability to detect cancer at its nascent stage compared to traditional methods, ensuring that even minor tumors that could escalate into interval cancers are identified promptly.

However, Lång emphasizes that this study primarily aimed to assess whether AI performs comparably to standard screenings, not necessarily to determine if it is superior, indicating that additional research is essential to validate AI’s efficacy.

The research did not assess performance across various ethnic groups, an area that current clinical trials in the UK aim to explore, according to Gilbert.

Moreover, further studies should investigate whether less experienced radiologists achieve similar benefits using AI-assisted technology, although Gilbert does not anticipate significant differences.

Following these promising results, there are plans to implement the AI approach in southwestern Sweden within a few months, while similar trials across other nations may take up to five years to assess the approach’s adaptability to diverse populations and screening frequencies, Gilbert noted.

Establishing the cost-effectiveness of the AI model is also critical. Current estimates suggest that if AI impacts screening positively, it may justify the investment, potentially reducing interval cancer incidences by at least 5%. Radiologists will require training; however, Lång believes that the simplicity of the software will facilitate this process.

It is vital to understand that even with advancements in AI technology, radiologist involvement remains essential in breast screenings. “Women participating in screenings prefer a human touch alongside AI, and I concur; it is crucial for radiologists to utilize AI as a supportive tool,” Lång emphasizes.

Topics:

Cancer /
Artificial Intelligence

Source: www.newscientist.com

Enhancing Cancer Treatment Efficacy with Fecal Transplants: A Promising Approach

Posted on January 29, 2026 by Igor Mitreski

Harnessing Gut Bacteria: A Novel Approach in Cancer Treatment

Lewis Houghton/Science Photo Library

For individuals unresponsive to conventional cancer therapies, fecal transplants from patients who have successfully undergone treatment could significantly enhance recovery odds. Modifying the gut microbiome impacts the immune response and has shown potential in stabilizing tumors during initial studies involving kidney cancer patients.

Fecal microbiota transplantation (FMT) is a safe procedure where a stool sample from one individual is transferred into another’s intestine to improve microbiome diversity. Initially approved to tackle recurring antibiotic-resistant Clostridioides difficile infections, FMT is on the rise in both the UK and US, and it has shown promise in conditions like irritable bowel syndrome.

While immunotherapy drugs, such as checkpoint inhibitors, enhance immune system functions to combat cancer cells, they may not be universally effective. Previous studies suggest that FMT from responding individuals could provide benefits for non-responders. “The microbiome significantly influences host immunity; thus, modifying it may enhance immune responses and facilitate cancer cell destruction,” states Gianluca Ianilo from the Catholic University of the Sacred Heart in Rome, Italy.

Prior research predominantly examined melanoma, a specific skin cancer, without comparing FMT effects to a placebo. To mitigate these gaps, Ianilo and colleagues enlisted 45 adults with kidney cancer who had commenced dual therapy with the checkpoint inhibitor pembrolizumab and axitinib—a medication obstructing tumor blood supply—within the last two months.

Participants were randomly split into two groups: one receiving FMT from a male donor whose cancer remitted post-checkpoint inhibitors, and the other receiving saline, both administered through a small tube rectally.

Following the initial transplant, most participants were given two additional doses (FMT or saline) three and six months later, but this time in oral pill form.

In the FMT cohort, participants maintained stable cancer status for an average of two years following the first transplant, contrasting with just nine months in the placebo group. Moreover, over half of those in the FMT group experienced tumor reduction, compared to approximately one-third in the placebo group.

“This provides robust evidence indicating that gut microbiome manipulation can significantly affect immunotherapy outcomes,” claims Hassan Zaroor from the University of Pittsburgh, Pennsylvania.

While the exact mechanism of FMT’s efficacy remains unclear, stool sample analyses taken before and after FMT indicate that FMT may introduce beneficial gut bacteria like Blautia wechslerae, which produce short-chain fatty acids that promote anti-cancer immune responses.

Additionally, FMT appeared to adjust the bacterial composition in recipients’ guts. For instance, it diminished levels of harmful strains like Escherichia coli, which trigger inflammation, while boosting beneficial bacteria like Ruminococcus bromii, known for enhancing growth of other beneficial bacteria that produce short-chain fatty acids.

This finding aligns with another recent study indicating that FMT can significantly enhance the effectiveness of checkpoint inhibitors in patients with non-small cell lung cancer compared to immunotherapy alone.

These trials suggest that FMT may also prove effective against additional tumor types responsive to checkpoint inhibitors, including those affecting the bladder and head and neck, although larger randomized controlled trials are necessary to validate these findings, according to Elkrief.

Future research must determine which specific bacterial strains confer benefits, potentially enabling the development of synthetic microbial preparations for widespread cancer treatments, Ianilo emphasizes.

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Source: www.newscientist.com

New Bone Cancer Treatment Shows Unexpected Reduction in Tumor Pain

Posted on January 23, 2026 by Igor Mitreski

Artist’s Impression of Nanomedicine in Action

Alfred Pasieka/Science Photo Library

Nanomedicine Concept Art — Artist’s Impression of Nanomedicine in Action

Alfred Pasieka/Science Photo Library

Cancer that metastasizes to the bones can be both deadly and painful. A new innovative drug is showing promise in addressing these issues by disrupting the interaction between tumors and nerves. This groundbreaking approach may lead to a much more comfortable cancer treatment journey.

According to William Fan from Harvard University, who was not part of the study, “This highlights a new and exciting paradigm in which a single cancer treatment can simultaneously improve mortality and quality of life.”

Research indicates that 65-80% of individuals with breast or prostate cancer ultimately develop bone cancer when the disease spreads. As these tumors progress, they irritate nearby pain-sensing nerves.

Standard treatments such as radiation therapy and chemotherapy are commonly utilized to shrink bone tumors. However, pain may still persist due to residual cancer cells interacting with nerves. Furthermore, conventional methods can harm healthy tissues and often require long-term use of painkillers, like opioids, risking addiction, as noted by Xian Jia Asia at Zhejiang University in China.

In response, Xian and colleagues have introduced a revolutionary “nanotherapy” comprising tiny fat capsules loaded with DNA that encodes gasdermin B, a protein designed to kill cancer cells selectively. This therapy targets cancer cells while sparing healthy ones, utilizing the characteristic higher levels of reactive oxygen species found in tumor cells. The nanocapsules additionally contain OPSA, which enhances the body’s inherent anti-cancer immune response.

To evaluate the efficacy of this novel drug, researchers injected breast cancer cells into the legs of various mice. Once bone tumors formed, the mice received either the full nanotherapy, a simpler version containing OPSA but lacking the gasdermin B gene, or a saline control. Treatments were administered into the tail every other day over five days.

After two weeks, tumors in the full nanotherapy group were on average 94% smaller than those in the control group, while the simpler form resulted in a 50% reduction. Furthermore, all mice treated with the complete nanotherapy survived, in contrast to merely 60% of those receiving the simpler therapy and 20% in the control group. This treatment effectively killed tumor cells and induced an anti-tumor immune response, Xiang reported.

Interestingly, both forms of the nanotherapy improved mobility in the affected limbs significantly more than the control, particularly in the full nanotherapy group, indicating potential pain relief from bone tumors. Tumor samples revealed a noticeable decrease in the density of nerve cells within the cancerous growths.

The mechanism appears to involve enhancing the cancer cells’ ability to absorb calcium ions, essential for nerve growth and pain signal transmission. “The concept is that cancer cells act like sponges for local calcium, reducing the availability of calcium for sensory neurons,” explains Professor Huang. Further studies are necessary to establish how nanotherapy adjusts calcium uptake in cancer cells, which may expose new avenues for targeting this critical pathway.

In preliminary findings, it was observed that nerves surrounding tumors could facilitate their growth, suggesting that nerve-related mechanisms could not only alleviate pain but also inhibit tumor proliferation, although specific impacts remain uncertain, according to Xiang.

These findings bolster the emerging perspective that targeting the nervous system may transform cancer treatment paradigms, states Huang. However, translating these treatments from mice to humans remains challenging due to differences in immune responses. Xiang aspires to initiate human clinical trials within five to ten years.

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Source: www.newscientist.com

How Bacteria and Viruses Collaborate to Combat Cancer: Insights from Sciworthy

Posted on January 22, 2026 by Igor Mitreski

The history of cancer can be traced back to ancient Egyptian civilizations, where it was thought to be a divine affliction. Over the years, great strides have been made in understanding cancer’s causes and exploring diverse treatment options, although none have proven to be foolproof. Recently, a research team at Columbia University has pioneered a novel method for combating cancerous tumors by utilizing a combination of bacteria and viruses.

The researchers engineered this innovative strategy by infecting bacterial cells with Typhimurium that were modified to carry the Seneca virus A. The theory posited that when tumor cells engulf these bacteria, they would also take in the virus, which would then replicate within the cells, leading to their death and the subsequent distribution of the virus to surrounding cells. This technique has been termed Coordinated Activities of Prokaryotes and Picornaviruses for Safe Intracellular Delivery (CAPPSID).

Initially, the research team verified that Typhimurium was a suitable host for Seneca virus A. They infected a limited number of these bacteria with a modified variant of the virus that emitted fluorescent RNA. Subsequently, they applied a solution that facilitated viral entry into the bacteria. Using fluorescence microscopy, they confirmed the presence of viral RNA inside the bacterial cells, validating the infection. To further assist the viral RNA in escaping the bacteria and reaching cancer cells, the researchers added two proteins, ensuring that viral spread was contained to prevent infection of healthy cells.

After optimizing the bacteria and virus, the team tested the viral delivery system on cervical cancer samples. They found that viral RNA could replicate both outside of bacterial cells and inside cancer cells. Notably, newly synthesized RNA strands were identified within tumor cells, confirming the successful delivery and replication of the virus through the CAPPSID method.

Next, the researchers examined CAPPSID’s impact on a type of lung cancer known as small cell lung cancer (SCLC). By tracking fluorescent viral RNA within SCLC cells, they assessed the rate of viral dissemination post-infection. Remarkably, the virus continued to propagate at a consistent rate for up to 24 hours following the initial infection, demonstrating effective spread through cancerous tissue without losing vigor.

In a follow-up experiment, the researchers evaluated the CAPPSID method on two groups of five mice, implanting SCLC tumors on both sides of their backs. They engineered the Seneca virus A to generate a bioluminescent enzyme for tracking purposes and injected the CAPPSID bacteria into the tumors on the right side. Two days post-injection, the right-side tumor glowed, indicating active viral presence. After four days, the left-side tumor also illuminated, suggesting that the virus had successfully navigated throughout the mice’s bodies while sparing healthy tissues.

The treatment continued for 40 days, leading to complete tumor regression within just two weeks. Remarkably, upon observation over a subsequent 40-day period, the mice demonstrated a 100% survival rate, with no recurrence of cancer or significant side effects. The research team observed that the CAPPSID virus, being encapsulated by bacteria, could circumvent the immune response, thus preventing cancer cells from building immunity against it.

Finally, to prevent uncontrolled replication of Seneca virus A, the researchers isolated a gene from a tobacco virus responsible for producing an enzyme that activates a crucial protein in Seneca virus A. By incorporating this gene into the Typhimurium bacteria, they were able to independently produce this enzyme, ensuring the virus could not replicate or spread without the bacteria’s presence. Follow-up tests confirmed that this modified CAPPSID method improved viral spread while maintaining confinement within cancer-affected areas.

The research findings hold promising potential for the development of advanced cancer therapies. The remarkable regression of tumors in mice and the targeted delivery system of CAPPSID—without adverse effects—could lead to safer cancer treatments for human patients, eliminating the need for radiation or harmful chemicals. However, the researchers also cautioned about the risk of viral and bacterial mutations that may limit the effectiveness of CAPPSID and cause unforeseen side effects. They suggested that enhancing the system with additional tobacco virus-derived enzymes could help mitigate these challenges, paving the way for future research into innovative cancer therapies.

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Source: sciworthy.com

U.S. mRNA Cancer Vaccines: Projected Costs Exceed $75 Billion

Posted on December 30, 2025 by Igor Mitreski

Significant Economic Benefits of mRNA Cancer Vaccines Currently Under Development

Eugene/Getty Images

In August 2025, the United States announced a $500 million cut in funding for vaccine development, jeopardizing the potential advantages of mRNA cancer vaccine research. According to Alison Galvani from Yale University and colleagues, this reduction poses significant risks to future developments.

The team’s analysis indicates that the treatment advancements observed in current clinical trials could prevent nearly 50,000 deaths, translating to an economic value of $75 billion. “This estimate is based on just one annual cohort of patients for each cancer type,” stated the researchers.

Experts caution that diminishing federal investment in mRNA vaccine technology risks undermining these crucial benefits.

Recent research highlights that many of the most effective cancer treatments leverage the body’s immune response to combat tumors. mRNA vaccines can specifically activate the immune system to identify proteins unique to cancer cells, offering a tailored approach to cancer treatment.

To evaluate the potential impact of these vaccines, Galvani and her team analyzed 32 ongoing mRNA cancer vaccine clinical trials in the U.S. They identified the top 11 promising trials and estimated the additional years of life these treatments could provide if widely administered to eligible patients within a year.

Furthermore, the researchers calculated the annual value of an additional year of life, utilizing statistical measures regarding how much individuals would pay for such benefits. They applied values established by the U.S. Department of Health and Human Services to assess the implications of potential regulatory shifts.

Although the annual estimates may be optimistic—given that some vaccine candidates may not gain approval—Oliver Watson from Imperial College London employed a similar framework, estimating that COVID-19 vaccines have yielded global health and economic benefits ranging from $5 trillion to $38 trillion.

If researchers evaluated the cumulative value of multiple cohorts receiving cancer treatments and extended their analysis over a longer time frame, the potential benefits would be substantially greater. “These estimates are undoubtedly conservative,” Watson notes.

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Source: www.newscientist.com

New Insights into How Exercise Can Help Slow Cancer Progression.

Posted on December 2, 2025 by

Exercise reduces cancer cell size in mice—possibly applicable to humans

Alfredas Pliadis/Xinhua News Agency/Alamy

Exercise has the potential to slow tumor development in mice by altering metabolic pathways, enabling muscle cells to absorb glucose instead of cancer cells for growth. This may also occur in humans.

While it’s established that exercise lowers cancer risk and healthier individuals generally have better cancer survival rates, the underlying mechanisms are still being explored. Notably, some benefits of exercise appear linked to changes in gut microbiota and the immune system.

To examine another possible pathway, Rachel Perry and her colleagues at Yale University School of Medicine conducted an experiment on 18 mice injected with breast cancer cells. Twelve of these mice were given an obesity-inducing diet, known to accelerate various cancers. Half of the group was also equipped with a running wheel to exercise as desired.

After four weeks, tumors in the exercising obese mice were found to be 60% smaller compared to their non-exercising counterparts, and were slightly smaller than tumors in sedentary mice fed a standard diet. The study revealed that just 30 minutes of exercise led to an increase in oxygen and glucose uptake in skeletal and cardiac muscles, with a corresponding decrease in glucose assimilation by tumors.

“This research demonstrates that aerobic fitness significantly alters the metabolic rivalry between muscle and tumor,” states Perry. “Crucially, the exercise was voluntary—these mice weren’t being forced to run like marathon athletes; they exercised as per their preference.”

The scientists evaluated gene expression and identified changes in 417 genes associated with vital metabolic pathways in mice due to exercise. This indicates that muscle tissue utilizes more glucose while tumor tissue absorbs less.

Specifically, a reduction in mTOR, a protein pivotal for cancer cell proliferation, shows potential for limiting tumor expansion, according to the researchers.

Perry anticipates that these metabolic patterns, which are similar across mammals, may extend to humans, even those without obesity. In fact, analogous gene activity shifts during exercise have been documented in cancer patients.

“This points to another mechanism illustrating how exercise fosters a cancer-suppressive environment,” mentions Rob Newton from Edith Cowan University in Perth, Australia. “We need to conduct clinical trials in humans, as there’s no clear reason to suspect it wouldn’t produce similar outcomes.”

Perry emphasizes that metabolism encompasses all tissues and is influenced by both the microbiome and immune responses. “These metabolic adaptations may bridge the connections between exercise, the microbiome, the immune system, and tumor progression,” she explains. “However, I’d be surprised if the positive implications of exercise stemmed from a single mechanism.”

This discussion also sheds light on why lower muscle mass heightens cancer mortality risk, as observed by Newton. “If your muscles preferentially absorb glucose, increasing muscle mass and regularly activating your muscles could yield significant advantages.”

He believes it’s crucial to view exercise not just as a lifestyle change but as an adjunctive anti-cancer intervention alongside other treatments. “Identifying primary environmental contributors to cancer is key, and we must formulate specific strategies to address them,” Newton concludes. “While enhancing cardiorespiratory fitness is beneficial, if a patient presents with notably low muscle mass, that should be prioritized with strength training.”

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Source: www.newscientist.com

Y Chromosome Loss: A Possible Factor in Lung Cancer Progression and Outcomes

Posted on November 20, 2025 by

Insights into the impact of Y chromosome loss on lung cancer treatment outcomes may guide therapeutic choices.

Dakuku/Getty Images

Research indicates that men diagnosed with the predominant type of lung cancer are more likely to lose the Y chromosome in their cells. This phenomenon has both pros and cons; while it can prevent the immune system from combating tumors, it also enhances the effectiveness of standard anti-cancer therapies.

As men grow older, their cells frequently undergo mutations, leading to the loss of the Y chromosome. In immune cells, this loss is believed to correlate with heart disease and decreased life expectancy. Additionally, there is growing evidence that cancer cells that lose the Y chromosome may influence symptom progression, with bladder cancer being the most thoroughly researched case.

The loss of the Y chromosome is a binary occurrence—it either happens or it doesn’t. However, the health implications seem to depend significantly on the proportion of specific cells that lack the Y chromosome.

The recent study initiated by Dawn DeMeo and her team at Brigham and Women’s Hospital in Boston, Massachusetts, investigated how Y-chromosome genes are expressed in a publicly available dataset of lung adenocarcinoma samples. Lung adenocarcinoma, the most common form of lung cancer, originates from the mucus-producing cells lining the airways. Enhanced understanding of the relationship between Y loss and various health issues has motivated researchers to delve deeper into gene expression studies, according to DeMeo.

The team discovered that cancer cells, in contrast to healthy lung and immune cells, often lack the Y chromosome. This occurrence is independent of whether the tissue donor is a smoker—despite smoking being linked to lung cancer and Y chromosome loss.

The loss of Y chromosomes appears to accumulate over time. “Certain groups demonstrate a higher rate of Y chromosome loss across a greater number of cells, and we observe significant Y chromosome loss in a large fraction of tumors,” stated John Quackenbush from Harvard University.

To comprehend the reasons behind this accumulation, researchers examined other genetic alterations in Y-negative cells. They found that the loss of a common set of antigens produced by cancer cells correlates with diminished expression levels. These antigens usually notify immune T cells that cancer cells are abnormal and should be targeted. The decreased expression allows Y-negative cancer cells to proliferate unchecked.

“This implies that as tumor cells lose their Y chromosome, they become increasingly adept at evading immune surveillance, suggesting a selection of tumor cells that escape immune detection,” Quackenbush explained. T cell counts were consistently lower in samples with Y loss compared to those retaining the Y chromosome.

Positive findings emerged when researchers analyzed data from 832 lung adenocarcinoma patients treated with the immune checkpoint inhibitor pembrolizumab, a medication designed to restore the body’s immune response against tumors by reversing T-cell suppression. The analysis confirmed that Y chromosome loss was linked to improved treatment outcomes.

“Patients experiencing LOY [loss of Y] are more responsive to checkpoint inhibitors,” noted Dan Theodorescu from the University of Arizona, who found similar results in bladder cancer, establishing validation against an entirely different dataset.

However, while loss of the Y chromosome is linked to shorter life expectancies for men compared to women, existing data suggests it does not impact survival in patients with lung adenocarcinoma. Further research is needed to explore how the effects of such mutations influence survival across different cancer types, according to Theodorescu. As our understanding advances, he believes that loss of Y could eventually serve as a biomarker for clinical decision-making.

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Source: www.newscientist.com

Breastfeeding Triggers Immune Cell Surge and May Offer Cancer Protection

Posted on October 21, 2025 by

Immune-related changes occur in the breast after breastfeeding

Svetlana Repnitskaya/Getty Images

Breastfeeding has long been linked to lowering the risk of breast cancer. However, the precise mechanisms behind this effect remain elusive. Recent studies reveal that women who breastfeed possess a higher presence of specialized immune cells in their breasts that might inhibit malignant immune cells.

Previous findings indicate that the risk of breast cancer, which is the second most prevalent cancer globally, decreases by 4.3% for each year of breastfeeding. This preventive effect appears to be particularly advantageous for older mothers.

The exact reasons remain partially understood, but are believed to involve alterations in breast tissue and hormonal exposure. To investigate further, Shereen Roy and colleagues at the Peter McCallum Cancer Center in Victoria, Australia, examined breast tissue from 260 women from diverse ethnic backgrounds, aged 20 to 70. These women varied in their maternal status and breastfeeding experiences, with none having previously been diagnosed with breast cancer.

“We discovered that breastfeeding mothers have a greater quantity of specialized immune cells known as CD8+ T cells, which can persist in breast tissue for decades after childbirth,” says Roy. “These cells serve as local defenders, poised to combat abnormal cells that may lead to cancer.” In certain instances, these cells remained present for up to 50 years.

The researchers also investigated mice, some of which underwent a complete cycle of pregnancy, lactation, and breast recovery during the weaning of their pups. Their mammary tissue was analyzed 28 days later, by which point the mammary glands had reverted to their pre-pregnancy state. Other mice had their pups taken away shortly after birth, or they were not pregnant at all.

The study revealed that completing a full lactation cycle significantly increased the accumulation of specialized T cells in mammary tissue, a phenomenon not observed in the other mice. When triple-negative breast cancer cells, known for their aggressive nature, were transplanted into the mammary gland tissue, tumors developed much more slowly in mice that had experienced lactation. However, depleting these T cells led to rapid tumor growth.

The researchers also analyzed clinical data from over 1,000 women diagnosed with triple-negative breast cancer post at least one full-term pregnancy. They found that women who breastfed exhibited tumors with a higher density of CD8+ T cells. “This indicates that the body’s immune response against breast cancer is active and ongoing,” notes Roy.

After considering other risk factors linked to breast cancer mortality, such as age, the researchers noted that women who breastfed had substantially longer overall survival. However, the variability in the data made it challenging to determine whether the duration of breastfeeding impacted this outcome.

The research team believes that T cells accumulate during breastfeeding to fend off infections that can lead to mastitis. Additionally, the relationship between pregnancy and breast cancer is complex, with studies indicating the risk being mitigated primarily for pregnancies occurring at younger ages.

“These findings have significant implications for understanding why certain women possess a more inherent protection against aggressive breast cancer and how we might develop targeted prevention and treatment strategies in the future,” Roy explains. However, she emphasizes that the choice to breastfeed is personal, not feasible for everyone, and may not always prevent breast cancer development.

Daniel Gray, along with researchers from the Walter and Eliza Hall Medical Research Institute in Victoria, highlighted that one of the study’s strengths was the analysis of multiple groups of women. “This lays the groundwork for future research that may elucidate how CD8+ T cells retain ‘memory’ of breastfeeding,” he comments.

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Source: www.newscientist.com

New mRNA Vaccine May Enhance Immune Response and Aid Cancer Survival

Posted on October 19, 2025 by

mRNA vaccines show growing potential to revolutionize healthcare

Joseph Prezioso/AFP via Getty Images

The mRNA COVID-19 vaccination seems to offer an unexpected advantage: it may extend the lives of cancer patients by enhancing immunotherapy effectiveness.

A study analyzing about 1,000 individuals undergoing treatment for advanced skin and lung cancer revealed that those who received an mRNA COVID-19 vaccine within 100 days of starting treatment with an immune checkpoint inhibitor had nearly double the survival time compared to those who did not receive the vaccine during this period. Clinical trials to validate these findings are set to commence by year-end.

“The outcomes were astonishing,” states Elias Sayur, a researcher at the University of Florida. They speculate about the potential to develop an mRNA vaccine that enhances this immune response. “Could we craft a universal mRNA vaccine that activates the immune system across all cancer patients?” he muses. “The possibilities are extensive.”

However, is it advisable for someone just commencing checkpoint inhibitors to get a COVID-19 vaccine to improve treatment efficacy? “I am hesitant to provide clinical recommendations without concrete proof,” Sayur cautions. “Attempting to harness your immune system against cancer also carries risks,” he adds, urging adherence to established vaccine guidelines.

The rationale behind this finding lies in the immune system’s capacity to eliminate many cancers even before they escalate. Yet, some tumors evolve to obstruct this response. They achieve this by manipulating the “off switch” of T cells, which are responsible for destroying cancer cells. A well-known off switch is the protein PD-1 found on T cell surfaces.

PD-1 becomes inactive when it binds to a protein called PD-L1 on certain cell surfaces. This serves as a safety mechanism for cells to signal, “cease the attack, I am benign.”

Numerous cancers hijack PD-L1 by producing it in excessive amounts. Checkpoint inhibitors function by preventing PD-1 and other off switches from becoming activated. These treatments have significantly increased survival rates for conditions like lung cancer and melanoma, earning a Nobel Prize for their developers in 2018.

However, the efficacy of checkpoint inhibitors varies significantly. When an individual’s immune system fails to react to the tumor by dispatching T cells for an attack, these drugs offer limited benefit.

Consequently, combining checkpoint inhibitors with vaccines that bolster the immune system’s tumor combat capabilities could prove to be more effective than either strategy used in isolation. Cancer vaccines are generally tailored to elicit a response to mutated proteins in cancer cells and are often personalized. “We are attempting to discern the unique aspects of their tumors,” Sayur explains. “It demands substantial time, funding, and complexity.”

During cancer vaccine trials, his team observed that the non-specific mRNA vaccine used as a control also exhibited remarkable effectiveness. “It was an absolute surprise,” Sayur remarks.

In July, Sayur and colleagues published findings indicating that mRNA vaccines enhance anti-tumor responses, even when not aimed at cancer-specific proteins, as revealed in studies in mice. Vaccines can initiate an innate immune response that acts like an alarm, energizing the immune system and prompting T cells to move from tumors to lymph nodes, where they rally other immune cells for a focused attack.

Recognizing this potential, Sayur and his team examined the medical records of patients treated at the University of Texas MD Anderson Cancer Center.

Out of 884 advanced lung cancer patients receiving checkpoint inhibitors, 180 had received mRNA COVID-19 vaccinations within 100 days of initiating treatment. Those vaccinated survived for approximately 37 months, contrasting with roughly 20 months for those unvaccinated.

Furthermore, among 210 individuals with melanoma that had metastasized, 43 had been vaccinated within 100 days of starting checkpoint inhibitors. They had a survival time of around 30 to 40 months, compared to around 27 months for individuals who were not vaccinated in that time frame. Some vaccinated individuals remained alive at the time of analysis, indicating their survival may extend even longer. The research findings were shared at the European Society of Medical Oncology Congress in Berlin, Germany.

Previous reports have suggested that after receiving an mRNA COVID-19 vaccine, a proportion of tumors exhibited shrinkage, indicating potential anti-tumor effects in certain cases even without checkpoint inhibitors. “It’s certainly a possibility, but further investigations are essential to fully understand,” comments Sayur.

The United States recently declared significant cuts in funding for mRNA vaccine development, despite the substantial benefits they have provided during the pandemic and the vast potential they hold for treatments beyond vaccines.

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Source: www.newscientist.com

Early Findings Indicate Elevated Risk of Colon Cancer in Long-Distance Runners

Posted on September 20, 2025 by Igor Mitreski

Researchers may have identified a potential connection between extreme endurance running and colorectal cancer, as nearly half of marathon and ultra-marathon participants have undergone screening.

Initial research assembled 100 long-distance runners aged 35-50 for colonoscopy, though these findings have not yet been peer-reviewed.

Close to 50% were found to have polyps (growths), with 15% diagnosed with advanced adenomas—growths that are likely to progress to cancer.

In contrast, recent studies indicate that only about 4.5 to 6 percent of adults in their late 40s from the general population have these advanced adenomas. However, it’s important to note that these studies included significantly larger sample sizes.

“I was quite concerned when I observed a group of ultra-marathon runners in their 30s diagnosed with stage 4, very advanced colorectal cancer,” said Dr. Timothy Cannon, who led the study at the Inova Schar Cancer Institute in Virginia. BBC Science Focus.

“They reported experiencing bleeding and convulsions post-race. At least one or two mentioned that they were told this was normal following their runs.”

Such symptoms can result from ischemic colitis, where blood flow is diverted from the colon to supply oxygen to the legs and other muscles during intense activity. This can lead to swelling and bleeding but typically resolves spontaneously.

Dr. Cannon speculated whether repeated cycles of damage and healing could create conditions conducive to cancer development.

Blood flow to the legs deprives the intestines of oxygen.

“There is currently no evidence that ischemic colitis directly causes cancer,” he stated. “However, it’s not difficult to imagine the potential outcomes. When numerous cells die and regenerate chaotically, there are ample chances for DNA replication errors.”

Alternative explanations exist as well. Endurance athletes are known to possess distinct gut microbiota compared to non-runners, and they often consume considerable amounts of ultra-processed foods, such as bottled energy drinks.

Dr. Cannon’s team is preparing to compare the gut bacteria of runners with and without adenomas to that of non-runners.

The findings were presented at the American Society of Clinical Oncology’s annual meeting, yet researchers cautioned that these are merely preliminary results, necessitating further investigation. They also highlighted that the screening study lacked a control group of non-runners.

“This leans more toward hypothesis than definitive answers,” Cannon remarked.

“I definitely don’t want people to walk away thinking exercise is harmful because it is beneficial overall. The inquiry is whether high levels of exercise could elevate the risk of colon cancer—and I believe they might.”

Read more:

Running slowly may be essential for a healthier, longer lifespan. Here’s why
What are the limits of human endurance?
The astonishing truth about how running can alter one’s perception of time

Source: www.sciencefocus.com

Cancer Cells Manipulate Immune Proteins to Evade Treatment – Sciworthy

Posted on September 1, 2025 by Igor Mitreski

Cancer arises from the proliferation of abnormal, uncontrolled cells that create dense masses, known as Solid Tumors. These cancer cells possess unique surface markers called antigens that can be identified by immune cells. A crucial component of our immune system, T cells, carry a protective protein known as FASL, which aids in destroying cancer cells. When T cells encounter cancer antigens, they become activated and initiate an attack on the tumor.

One form of immunotherapy, referred to as chimeric antigen receptor T cell therapy or CAR-T therapy, involves reprogramming a patient’s T cells to recognize cancer cell antigens. However, CAR-T therapy often struggles with solid tumors due to the dense, hostile environment within these tumors, which obstructs immune cells from infiltrating and functioning effectively.

Another significant hurdle that clinicians encounter when treating solid tumors is their heterogeneous composition of various cancer cell types. Some of these cells exhibit antigens recognizable by CAR-T cells, while others do not, complicating the design of CAR-T therapies that can target all tumor cells without harming healthy cells. Solid tumors also produce the protein Plasmin, which further impairs the immune system’s ability to break down FASL and eliminate cancer cells.

Researchers from the University of California, Davis investigated whether shielding FASL from plasmin could preserve its cancer-killing capabilities and enhance the efficacy of CAR-T therapy. They found that the human FASL protein contains a unique amino acid compared to other primates, making it more susceptible to degradation by plasmin. Their observations suggested that when FASL was cleaved, it lost its ability to kill tumor cells. However, after injecting an antibody that prevents plasmin from cleaving FASL, it remained intact and preserved its cancer-killing function.

Since directly studying cell behavior in the human body poses challenges, scientists culture tumor cells and cell lines in Petri dishes under controlled laboratory environments. To gain insights into plasmin’s role, the team examined ovarian cancer cell lines obtained from patients, discovering that CAR-T resistant cancer cells exhibited high plasmin activity.

They noted that combining ovarian cancer cells with elevated plasmin levels with normal cells displaying surface FASL diminished FASL levels in the normal cells. When they added FASL-protecting antibodies, CAR-T cells effectively eliminated not only the targeted cancer cells but also nearby cancer cells lacking the specific target antigen. These findings indicated that plasmin can cleave FASL in T cells and undermine CAR-T therapy, suggesting that safeguarding FASL may enhance CAR-T treatment’s effectiveness.

To assess whether tumor-generated plasmin can deactivate human FASL in more natural settings, researchers examined its function in live tumors within an active immune system. They implanted ovarian, mammary, and colorectal tumor cell lines from mice into genetically matched mice to elicit a natural immune response. When human FASL protein was directly injected into mouse tumors, the cancer cells remained intact. In contrast, injecting a drug that inhibits plasmin resulted in cancer cell death. Additionally, administering FASL-protecting antibodies also led to the elimination of cancer cells.

As a final experiment, the team aimed to determine whether activated T cells from the mice’s immune systems could penetrate the tumors and kill cancer cells. They implanted mice with both plasmin-positive and plasmin-negative tumors, treating both with drugs to enhance immune cell activity and boost FASL production.

They discovered that in tumors with low plasmin levels, mouse immune cells expressed high amounts of FASL on their surfaces, while in tumors with elevated plasmin levels, FASL was significantly reduced. Once again, injecting FASL-protected antibodies into these tumors increased FASL levels. The researchers concluded that plasmin can diminish the immune system’s ability to eliminate cancer cells by depleting FASL from immune cells.

In summary, the team found that tumors exploit plasmin to break down the protective protein FASL, evading immune system attacks. Based on their findings, they proposed that plasmin inhibitors or FASL-protected antibodies could augment the effectiveness of immunotherapy in treating cancer.

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Source: sciworthy.com

Ex-Michigan Student Claims He Developed Cancer After Using Chemistry Program Labeled “Harmless”

Posted on August 19, 2025 by Igor Mitreski

A former Michigan graduate student is taking action against the university, claiming that her thyroid cancer is linked to her time there. She stated that her exposure to pesticides was deemed “harmless,” according to her and her legal team’s claims made on Monday.

Linglong Wei was diagnosed with thyroid cancer on June 26th of last year, attributing her condition to her experiences at MSU between 2008 and 2011 in a lawsuit filed in Ingham County Circuit Court.

According to the civil suit, “In Wei’s field studies, Michigan State University required her to apply excessive amounts of harmful pesticides and herbicides.”

Wei alleges exposure to several herbicides, such as dichloride, glyphosate, and oxyflufen, noting that they are linked to cancer.

The lawsuit claims Wei was not adequately trained and did not receive the necessary protective gear to handle such hazardous substances.

Looking back, Wei criticized the university for failing to implement stronger safety protocols.

“During my time as a student at MSU, I voiced my concerns, but no one listened,” Wei told reporters in Lansing.

“I felt afraid due to the department’s reactions. I didn’t strongly advocate for my safety, especially when I was told that exposure was safe.”

Wei, an international student from China, mentioned that the cancer left lasting marks on her throat, and she worries about her prospects of having children.

She speculated that MSU ignored her concerns.

“International students often feel overlooked, assuming their time here is temporary and their concerns go unheard,” Wei stated.

Maya Green, a former student lawyer, highlighted her client’s inadequate training and safety equipment provided by MSU.

“She was made to handle dangerous pesticides without proper gloves, protective equipment, breathing masks, or sufficient training,” Green said.

“Wei was placed in a position to handle these harmful substances without protection. She was a foreign student, navigating MSU’s system in a language that was not her own.”

The former Michigan student is seeking $100 million in damages.

“Wei was consistently assured that her activities posed no harm, and she relied on that assurance, only to suffer as a result,” her attorney noted.

Michigan State spokesperson Amber McCann declined to comment on the specifics of Wei’s case.

“While we cannot discuss ongoing litigation, we want to stress that Michigan State prioritizes the health and safety of the campus community,” McCann stated.

“We ensure that necessary training and personal protective equipment are provided in accordance with relevant university policies and state and federal regulations.”

Source: www.nbcnews.com

Common Artificial Sweeteners May Disrupt Cancer Treatment

Posted on July 31, 2025 by Igor Mitreski

Some artificial sweeteners can alter the gut microbiota composition, influencing overall health.

Ian Allenden/Aramie

SEI 260736834 — Some artificial sweeteners can alter the gut microbiota composition, influencing overall health.

Ian Allenden/Aramie

Individuals who consume the artificial sweetener sucralose may have reduced responsiveness to cancer immunotherapy, indicating that sweeteners could diminish treatment efficacy.

Immunotherapy enhances the immune system’s ability to identify and eliminate cancer cells, proving vital for many cancers. “When successful, it is highly effective. Patients can feel better, enjoy their lives, and survive for years,” states Abigail over Eichaldergoff from the University of Pittsburgh, Pennsylvania. “Regrettably, not all patients respond well; many cancer types benefit only a limited number of individuals.”

The reasons behind this are unclear, but numerous studies indicate that the gut microbiota plays a critical role in regulating immune responses; prior research has also demonstrated that artificial sweeteners can modify human gut microorganisms.

Consequently, Overacre and colleagues investigated the potential effects of artificial sweeteners on immunotherapy outcomes. They tracked the treatment results of 157 patients who underwent cancer immunotherapy for a minimum of three months. Among these, 91 had advanced melanoma, 41 had non-advanced non-small cell lung cancer, and 25 had melanoma that had been surgically excised but were at risk of recurrence.

Prior to treatment commencement, participants filled out a dietary questionnaire covering the previous month, enabling researchers to estimate their artificial sweetener intake.

Consumption exceeding 0.16 milligrams of sucralose per kilogram daily correlated with poorer treatment outcomes. Participants with advanced melanoma who ingested lower amounts of sucralose experienced longer survival rates, approximately five months more without cancer progression.

In the case of non-small cell lung cancer participants, the survival advantage was about 11 months. For those at higher risk of melanoma recurrence, reducing sucralose intake allowed them to remain cancer-free an additional six months compared to heavier consumers.

Similar outcomes were noted for participants who consumed more than 0.1 milligrams per kilogram daily of Acesulfame K, another artificial sweetener.

The US Food and Drug Administration (FDA) advises limiting sucralose intake to below 5 milligrams per kilogram daily. “Thus, the threshold which seems to reduce the effectiveness of immunotherapy is not half, or even 25%, but rather about 5% of the recommended daily amount,” states Diwakar Dabar from the University of Pittsburgh. “This suggests that even a small amount could have a detrimental effect.”

Additional experiments with mice bearing various types of tumors demonstrated that adding sucralose to their water during immunotherapy expedited tumor growth and decreased survival rates.

Genetic analysis revealed that immune cells activated by immunotherapy were less effective in mice provided with sucralose to combat cancer. Fecal analyses also indicated significant alterations in the rodent gut microbiota, notably increased activity in the metabolic pathway utilized by T cells to process arginine, a crucial amino acid.

The findings imply that sucralose may hinder immunotherapy by reducing arginine levels and modifying gut microbiota in ways that impair T-cell efficacy. Furthermore, experiments demonstrated that arginine supplementation improved survival rates in mice consuming sucralose, bringing them in line with those not consuming artificial sweeteners.

However, it remains uncertain if sucralose exerts similar effects on human gut microbiota and T-cell function. Josam Suez from Johns Hopkins University in Maryland notes, “It is incredibly challenging to derive findings based solely on human data, particularly regarding nutrition and food frequency surveys, while isolating specific impacts of non-nutritive sweeteners and isolating the effects of sucralose on clinical outcomes.”

“We invest considerable resources in the development of new medications, which is costly, challenging, and time-consuming,” remarks Davar. Discovering ways to enhance existing treatments, such as avoiding artificial sweeteners or using arginine supplements, presents a more straightforward and economical approach.

Nonetheless, further investigation is essential to determine if it genuinely enhances patient outcomes. “Hence, it is crucial to maintain support for these research priorities in a challenging funding landscape,” concludes Davar.

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Source: www.newscientist.com

COVID-19 and Flu Could Reactivate Dormant Lung Cancer Cells

Posted on July 31, 2025 by Igor Mitreski

Lung tissue samples from mice, depicting cells (blue), cancerous cells (green), and proliferation markers (magenta)

Bryan Johnson

Respiratory viruses are capable of triggering the growth of dormant cancer cells that have metastasized to the lungs from other body areas. Infectious diseases, such as influenza, can instigate an inflammatory response that aids the immune system in combating pathogens, yet they may also adversely influence cancer progression.

Cancer fatalities frequently result from tumor cells migrating from their primary sites. These cells may remain dormant in new locations for extended periods—potentially years or decades—before forming detectable tumors.

While it is uncertain if these cells will eventually proliferate, previous studies have suggested that once cancer cells infiltrate the lungs, inflammation induced by respiratory virus infections might play a significant role. “Nevertheless, no comprehensive research has been conducted to establish a clear cause-and-effect relationship,” notes James DeGregori from the University of Colorado.

To address this research gap, DeGregori and his team employed genetically modified mice to develop tumors in their mammary glands. By two months of age, each mouse had developed a mammary tumor and fewer than ten dormant cancer cells in their lungs.

Subsequently, the researchers infected half of the mice with the H1N1 influenza strain, commonly referred to as swine flu, causing illness for approximately two weeks. During the nine days following the infection, the number of lung cancer cells surged by 100-fold, whereas uninfected mice exhibited minimal changes.

In complementary experiments, the team discovered that the SARS-CoV-2 virus, responsible for COVID-19, led to a tenfold increase in cancer cell numbers in the mice’s lungs, again with no significant alterations in uninfected counterparts.

The researchers hypothesized that this expansion occurred due to viral infections elevating the levels of inflammatory molecules known as IL-6.

To investigate this hypothesis, they conducted further experiments with genetically modified mice deficient in IL-6 and found significantly fewer lung cancer cells compared to typical mice with normal IL-6 levels.

Another experiment suggested that IL-6 seemed to rejuvenate dormant cancer cells that had already migrated to the lungs instead of promoting the dissemination of these cells from the breasts.

However, IL-6 levels wane when the infection subsides. At this juncture, the researchers observed that cancer cells in the mouse lungs had ceased to proliferate but had acquired alterations in gene expression typically associated with tumor metastasis, according to DeGregori.

These findings suggest a potential impact on individuals with undetected levels of cancer cells in the lungs who are believed to be in remission, as stated by Anne Zeuner at the National Institutes of Health in Rome, Italy.

To determine the relevance of these findings to humans, researchers analyzed health records from 36,800 women in the U.S. diagnosed with breast cancer before the COVID-19 pandemic, who were thought to be non-metastatic.

Women who tested positive during the initial three years of the outbreak were significantly more likely to receive a diagnosis of secondary lung cancer in that timeframe. However, some women may have avoided testing due to asymptomatic infections, while others might not have sought tests, thereby complicating the validation of this finding, notes DeGregori.

Further research is necessary to corroborate these findings and explore the interactions between various respiratory viruses and cancer types, according to Zeuner. “Individual factors are likely to significantly influence the relationship between respiratory infections and cancer recurrence,” she adds.

The research focused solely on swine flu and SARS-CoV-2, but DeGregori expresses hope that a spectrum of viruses will exhibit similar behaviors, as many are known to elevate IL-6 levels. He also underscores the importance of vaccination, stating, “As a cancer survivor, I would ensure I am protected against common respiratory viruses like influenza and COVID-19,” remarks DeGregori.

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Source: www.newscientist.com

Could Cancer Medications Pave the Way for Alzheimer’s Treatment?

Posted on July 21, 2025 by Igor Mitreski

As treatment options for Alzheimer’s disease remain limited, researchers are exploring the repurposing of cancer medications to address cognitive decline.

The incidence of Alzheimer’s is on the rise due to an aging global population, yet no cure currently exists. Efforts to discover new therapies that can halt the progression of the disease instead of merely managing symptoms have often been unsuccessful.

At present, only two medications, Leqembi and Kisunla, have received FDA approval to slow the progression of early Alzheimer’s disease, and the extent of their effectiveness is considered limited.

Several pharmaceutical firms have either shelved or discontinued their Alzheimer’s drug development initiatives after encountering trial failures. Others are investigating the potential of established medications, including popular weight loss drugs in combating the disease.

In this context, researchers at the University of California, San Francisco, conducted extensive screenings of existing drugs that could be repurposed for Alzheimer’s treatment, aiming to shorten the time required for patient access to these drugs. They analyzed a database of over 1,300 different medications, spanning various drug classes such as antipsychotics, antibiotics, antifungals, and chemotherapeutics, and assessed their impact on gene expression.

Their recent study, published in the journal Cell, pinpointed two cancer drugs as the leading candidates to potentially mitigate the risk of Alzheimer’s in patients. When used in combination, these drugs demonstrated the ability to slow or even reverse Alzheimer’s symptoms in mouse models. One of the medications is typically used for breast cancer treatment, while the other targets colon and lung cancers.

Significant alterations in gene expression in the brain are characteristic of Alzheimer’s disease, leading to the increased synthesis of certain proteins and decreased production of others. These disruptions can impair brain functionality and result in symptoms such as memory loss.

According to the researchers, the two drugs, identified from a database of nearly 90, were able to reverse the expression of genes associated with Alzheimer’s in human brain cells. Furthermore, based on electronic medical records, five specific drugs appeared to lower Alzheimer’s risk among actual patients, ultimately leading the authors to select two FDA-approved cancer treatments for animal testing.

“We were not anticipating that cancer medications would emerge as strong contenders,” remarked Marina Sirota, interim director of the UCSF Bakar Computational Health Sciences Institute.

The authors noted that letrozole, a breast cancer treatment, seems to modify gene expression within neurons, while irinotecan, a colon cancer medication, appears to influence gene expression in glial cells that support the nervous system. Alzheimer’s disease leads to nerve cell destruction, excess glial cell proliferation, and brain inflammation.

A 2020 study indicated that breast cancer patients treated with letrozole had a lower incidence of Alzheimer’s disease compared to those who did not receive the drug. Similarly, colorectal cancer survivors who were administered irinotecan exhibited a reduced risk of Alzheimer’s disease, as noted in research from 2021.

After evaluating the drugs in mice, the study authors discovered that the combination of the two medications reversed cognitive decline and enhanced memory in mice displaying traits of Alzheimer’s disease as they aged.

Given that results observed in mice do not always have a direct correlation with human outcomes, researchers aim to conduct clinical trials with Alzheimer’s patients.

“The development of new medications typically incurs costs in the millions, often billions, and can span over a decade. In contrast, repurposed medications may require only two to three years and carry significantly lower costs to reach clinical trial stages,” Sirota explained.

“Currently, we are not producing highly effective treatments that can significantly decelerate cognitive decline,” she added.

The challenge in developing Alzheimer’s treatments lies in the intricate nature of the disease, with its exact causes remaining largely elusive.

At this point, the authors admit that the precise mechanisms by which cancer drugs may be effective against Alzheimer’s are uncertain. One hypothesis suggests that breast cancer medications inhibit estrogen production—a hormone that regulates the expression of numerous genes. Colon cancer drugs might mitigate brain inflammation by preventing glial cell proliferation, yet Huang notes that there could be additional explanations.

Dr. Melanie McReynolds, a biochemistry assistant professor at Penn State University who was not involved in the research, offered another perspective.

She suggested that the study indicates various cancer drugs may prove beneficial in treating Alzheimer’s by modulating glucose metabolism, the process by which cells generate energy. McReynolds emphasized that this process is vital for communication among different brain cells.

“Aging, stress, and illness can disrupt that communication,” she stated.

McReynolds expressed that the drug combinations evaluated in the current research have the potential to reverse metabolic declines.

However, it is crucial to understand how Alzheimer’s patients will respond to these cancer drug combinations. Letrozole can induce hot flashes, while irinotecan is known for causing severe diarrhea. Both treatments may also lead to nausea and vomiting.

“These medications come with significant side effects, so it’s essential to weigh these risks carefully and determine whether such side effects are manageable for individuals with Alzheimer’s,” stated Sirota. “It’s not a straightforward solution.”

Source: www.nbcnews.com

Rising Rates of Gastrointestinal Cancer Among Individuals Under 50

Posted on July 17, 2025 by Igor Mitreski

Rising Rates of Gastrointestinal Cancer in Young Adults

Gastrointestinal cancers, which encompass colorectal, gastric, and pancreatic cancers, are increasingly prevalent among young adults, though the reasons remain largely unclear. The potential causes warrant further investigation, according to experts. A review published in JAMA on Thursday highlights that gastrointestinal cancer has become the fastest-growing cancer among adults under 50 in the United States.

This review offers one of the most comprehensive overviews of gastrointestinal cancer trends, synthesizing data from a major international cancer database alongside 115 studies published from January 2014 to March 2025. The authors stress the importance of adhering to colorectal cancer screening guidelines. They recommend that individuals at average risk begin screening—typically through colonoscopy or stool tests—at age 45. As screening for pancreatic, stomach, and esophageal cancers remains infrequent in the U.S., the authors are exploring innovative ways to broaden screening access.

“This underscores the necessity of improving screening and early detection,” stated Dr. Kimmie Ng, co-author and director of the Dana-Farber Cancer Institute’s Young Onset Colorectal Cancer Center.

According to the findings, colorectal cancer is the most frequently diagnosed early-onset gastrointestinal cancer, with approximately 185,000 cases worldwide in 2022, including nearly 21,000 in the U.S. This reflects a 2% annual increase since 2011, as reported by the American Cancer Society. “This is unprecedented in this age group, and we are witnessing a significant rise among individuals in their 20s, 30s, and 40s,” commented Dr. John Marshall, chief medical consultant for the nonprofit Colorectal Cancer Alliance, which was not involved in the study. A notable case is actor Chadwick Boseman, who was diagnosed with colon cancer in 2016 and passed away at age 43 four years later.

Emerging research indicates a rise in early-onset cases of pancreatic, stomach, and esophageal cancers as well. Previous studies suggest that the incidence of these gastrointestinal cancers is disproportionately higher among Black and Hispanic populations. Pancreatic cancer, known for its high mortality rate, shows that only 13% of patients survive five years post-diagnosis. Although colorectal cancer is the most common, healthcare providers possess a better understanding of the factors contributing to early-onset cases compared to other cancers.

“Understanding the dynamics of colorectal cancer has given us insights into its initiation,” noted Dr. Scott Kopetz, a professor of gastrointestinal medical oncology at the University of Texas MD Anderson Cancer Center. He posited that multiple factors likely contribute to the increase in early-onset cases. “There isn’t one overarching theory,” he said.

The recent review in JAMA suggests that lifestyle factors such as obesity, sedentary behavior, inadequate nutrition, tobacco use, and alcohol consumption are largely associated with early-onset gastrointestinal cancers. A specific study highlighted that women who consumed more sugary beverages during puberty faced a heightened risk of developing early-onset colorectal cancer. “The behaviors and exposures during childhood and adolescence likely contribute to the cancer risks seen in young adults,” remarked Dr. Ng.

Health Secretary Robert F. Kennedy Jr. has raised concerns about the correlation between sugary drinks and health issues, including cancer. Recently, President Donald Trump announced that Coca-Cola would switch to cane sugar instead of U.S. corn syrup; however, the company did not confirm this change to NBC News.

Dr. Marshall speculated that the uptick in early-onset colorectal cancer may be linked to shifts in gut microbiota. Factors such as diet, antibiotic usage, microplastics, and chemical exposures could impact these bacteria, yet scientists lack a clear understanding of what constitutes a healthy microbiome and its implications for health. This area is ripe for research.

The review by Dr. Ng found that between 15% and 30% of individuals with early-onset gastrointestinal cancer carry hereditary genetic mutations, indicating a propensity to develop cancer earlier. She advocates for genetic testing for all patients diagnosed under 50.

Despite improvements in treatment and screening that have boosted overall survival rates for gastrointestinal cancer, the review indicates that younger patients often experience poorer outcomes. This trend persists despite receiving more comprehensive treatment, including surgeries, radiation, and aggressive chemotherapy regimens. One reason cited is that primary care physicians may overlook symptoms such as abdominal pain, constipation, heartburn, and reflux in younger patients, delaying diagnosis.

“In my experience, when young individuals present with non-specific symptoms, there tends to be a lack of consideration for colorectal or other gastrointestinal cancers, leading to more advanced-stage diagnoses,” said Dr. Howard Hochster, director of gastrointestinal oncology at Rutgers Cancer Institute and RWJBarnabas Health. However, Dr. Ng pointed out that younger patients still display worse survival rates, even when accounting for the stage of diagnosis. “This leads us to contemplate whether cancers that arise in younger individuals might possess unique biological characteristics that render them more aggressive or less responsive to treatment,” she concluded.

Source: www.nbcnews.com

Exercise Fights Cancer: Uncovering the Reasons Behind It

Posted on July 9, 2025 by Igor Mitreski

Exercise appears to have a cancer-fighting effect

Franziska & Tom Werner/Getty Images

Physical activity is recognized for its role in cancer prevention and in inhibiting the growth of existing tumors. It’s also linked to alterations in gut microbiota. Recent research illustrates how these alterations can empower exercise in the battle against cancer.

Marlies Meisel from the University of Pittsburgh and her team administered an aggressive form of melanoma to two groups of mice. One group followed a four-week exercise program, while the other remained inactive.

As anticipated, the active mice showed smaller tumors and better survival rates. However, in mice treated with antibiotics, exercise provided no benefits to those that were completely sterile. The findings revealed a significant role of microorganisms, with the beneficial molecules known as metabolites playing a crucial part.

Given that the microbiome generates thousands of metabolites, the researchers employed machine learning to analyze potential molecules, ultimately pinpointing a particular bacterial metabolite that surged with exercise. This metabolite enhances the effectiveness of CD8 T cells within the immune system, making it vital in the fight against cancer.

Furthermore, the team studied 19 individuals with advanced melanoma, discovering that those with higher levels of this metabolite exhibited longer survival rates compared to those with lower levels.

“This study underscores the significance of evaluating the metabolites produced by bacteria, rather than merely identifying the bacteria involved,” Meisel emphasizes.

Ken Lau, who studies the influence of the intestinal microenvironment on conditions like colorectal cancer and inflammatory bowel disease at Vanderbilt University in Tennessee, shares excitement for this type of research, as it offers insights into how to leverage specific molecular pathways to enhance the immune response. However, he cautions that further research is necessary. “What occurs when a patient stops exercising? Will the effects diminish or persist in some manner? There is still much to learn,” he states.

Meisel and her team are exploring whether the exercise-induced alterations in gut microbiota may influence other health conditions.

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Source: www.newscientist.com

Herpes Virus Could Be Fast-Tracked for Treating Severe Skin Cancer

Posted on July 9, 2025 by Igor Mitreski

Melanoma is a form of skin cancer that can metastasize

Science Photo Library

After years of research and extensive human trials, only one virus specifically engineered to target cancer has gained approval from US and European regulators. Following promising results in treating melanoma—a notably aggressive skin cancer—approval may soon be granted.

The genetically altered herpes virus, known as RP1, was injected into the tumors of 140 patients with advanced melanoma who did not respond to conventional treatments. All participants also received a medication called nivolumab, designed to enhance the immune response against the tumors.

In 30% of the treated individuals, tumors shrank, including those that were not directly injected. Notably, in half of these cases, the tumors were completely eradicated.

“Half of the patients who responded experienced a complete response, meaning total disappearance of all tumors,” said Gino Kim from the University of Southern California. “I am thrilled with these results,” he added, noting that other treatments for patients at this stage often perform poorly and have harsher side effects.

A larger trial involving 400 participants is currently in progress; however, RP1 may receive approval from the US Food and Drug Administration (FDA) to be used in conjunction with Nivolumab for treating advanced melanoma before the trial concludes. The New Scientist reports that “the FDA is anticipated to make a decision by the end of this month.”

For over a century, it has been recognized that viral infections can aid in cancer treatment, though intentionally infecting someone with a “wild” virus poses significant risks. In the 1990s, scientists attempted to genetically modify viruses to effectively target cancer while leaving healthy cells unharmed.

These engineered viruses function in two main ways: First, they directly invade cancer cells, causing them to rupture and die. Secondly, they stimulate immune responses aimed at all cancer cells present in the body.

For instance, T-VEC, a modified herpes simplex virus, was engineered to release an immune-boosting factor called GM-CSF within infected tumor cells. T-VEC received approval in 2015 in both the US and Europe for treating inoperable melanoma.

Unfortunately, T-VEC’s use is limited as it was only tested and approved for injection into skin tumors. Many patients with advanced melanoma have deeper tumor locations, as noted.

With RP1, the strategy shifted to administering it into deeper tumors. RP1, like T-VEC, is a herpes simplex virus but has undergone various enhancements. It notably aids in fusing tumor cells with adjacent ones, thus boosting viral spread within the tumor and reinforcing the immune response.

Though there have been no direct comparisons between T-VEC and RP1, RP1 demonstrates a greater likelihood of reducing all tumors, rather than just those directly injected. “It indicates a more pronounced systemic effect,” experts state.

Thus, should RP1 gain approval, its application is expected to be far broader than that of T-VEC. Experts believe this could significantly enhance the overall interest in utilizing cancer-targeting viruses. “There seems to be increasing enthusiasm for this approach.”

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Source: www.newscientist.com