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.

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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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Source: sciworthy.com

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.

Topics:

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

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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.

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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

Unexpected “Harmless” Microorganisms May Significantly Influence Colorectal Cancer

Posted on July 3, 2025 by Igor Mitreski

Methanobrevibacter shows that a microorganism named smithii is linked to colorectal cancer

Kateryna Kon/Science Photo Library/Alamy

Ancient mysterious microorganisms, distinct from bacteria and viruses, are believed to have a role in colorectal cancer, challenging the notion that these microorganisms are harmless.

Life can be categorized into three domains: the first consists of single-celled bacteria, the second includes eukaryotes—multicellular organisms such as animals and plants equipped with complex cells housing nuclei and DNA.

The third domain is Archaea, comprising single-celled organisms previously mistaken for bacteria due to their lack of nuclei. Recent findings reveal that they possess some traits similar to eukaryotes, suggesting that the first eukaryotes might have originated from archaeal cells that incorporated free-living bacteria.

Our intestines harbor trillions of bacteria and viruses linked to various conditions, including cancer, diabetes, obesity, and heart disease, alongside archaea, though the latter is often overlooked.

“Most researchers studying the human microbiome tend to overlook archaea, disregarding their potential significance,” notes Roxy Mohammadzadeh from Glaz Medical College in Austria. However, several archaea have been associated with colorectal cancer, Parkinson’s disease, infections related to gum disease, and urinary tract infections.

In pursuit of a clearer understanding, Mohammazzade and her team analyzed data from 19 clinical studies involving more than 1800 individuals.

They observed that while the link between archaea and several medical conditions is prevalent, it varies. Particularly, Methanobrevibacter smithii was notably present in individuals with colorectal cancer. This microbe significantly aids digestion by converting bacterial fermentation byproducts like hydrogen and carbon dioxide into methane.

Utilizing microbial culturing techniques, the team found M. smithii interacting with bacteria such as Bacteroides fragilis, E. coli, and Fusobacterium nucleatum.

These bacterial species have been linked to colorectal cancer; particularly, the association with F. nucleatum appears to be significant given its relationship with cancer. When M. smithii coexists with F. nucleatum, the latter produces higher amounts of succinate, a critical metabolic signaling molecule recognized for enhancing tumor invasiveness and spread potential noted in cancer studies.

“This represents the first mechanical evidence linking archaea to human diseases, particularly colorectal cancer,” states Mohamatzade.

This research reinforces earlier findings connecting M. smithii to colorectal cancer, asserting the need for further exploration to uncover the mechanisms at play and why this microorganism is prevalent in colorectal cancer patients, according to Gianmarco Piccinno from Trent University, Italy. He emphasizes that most available evidence is correlational and calls for additional studies.

“While Archaea is acknowledged as part of the human microbiota, its direct involvement in diseases remains poorly understood,” points out Sunny Wong from Nanyang Technological University in Singapore. Recent studies have also established connections between archaea and colorectal cancer. “Though they exist in fewer numbers than bacteria in the intestine, they are metabolically active, often consuming hydrogen, producing methane, and interacting with the host.”

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Source: www.newscientist.com

Gastric Bypass Surgery Potentially Lowers Intestinal Cancer Risk

Posted on June 26, 2025 by Igor Mitreski

Gastric bypass surgery is primarily utilized for weight loss, but it may provide other advantages

Portra/Getty Images

A widely recognized form of weight loss surgery may lower the risk of colorectal cancer by changing the levels of bile acids in the bloodstream. These findings could pave the way for new bowel cancer treatments.

During gastric bypass surgery, the stomach is surgically altered to create a small upper pouch and a larger lower pouch. The small intestine is then connected to the upper pouch, allowing food and digestive juices to bypass most of the upper stomach and small intestine. Post-surgery, patients often feel fuller and experience quicker weight loss.

Earlier research indicated that this procedure is associated with a decreased risk of colorectal cancer; however, the underlying reasons remained unclear. To investigate further, Rebecca Kesselling of the University of Freiburg, Germany, and her team fed mice a high-fat diet until they reached approximately 50% of their starting weight. They then performed a partial gastric bypass on some of the mice, while the remaining mice underwent a sham surgery that did not alter their digestive systems.

To isolate the weight-loss effects of gastric bypass surgery, the team grouped the gastric bypass mice alongside half of the sham-operated mice. Over six weeks, the gastric bypass mice lost about 20% of their body weight on average.

Subsequently, the researchers implanted colorectal cancer cells into the colons of the mice. After an additional six weeks, it was observed that colon tumors in the gastric bypass mice were two-thirds smaller than those in the mice that either continued gaining weight or lost weight solely through diet.

Additionally, cancer spread to the liver was seen in only one out of twenty gastric bypass mice, while it occurred in most of the sham-operated mice.

“Both sham groups exhibited similar tumor levels, but weight loss alone could not account for the lower cancer risk, suggesting that gastric bypass involves additional factors,” Kesselling explains.

The researchers speculated that this might be attributed to alterations in bile acids, which are compounds that aid in fat digestion. These molecules are typically produced by the liver, move through the gallbladder, stomach, and small intestine, and then return to the liver via the bloodstream.

“Bile acids are reintroduced into the small intestine during bypass surgery,” Kesselling states, implying that this process may lead to variations in intestinal bacteria that chemically modify these molecules.

The mice that underwent gastric bypass surgery displayed lower levels of specific bile acids, known as primary bile acids, in both their colon and bloodstream compared to the sham group.

To further explore whether changes in bile acids influenced cancer risk, the team conducted a similar experiment with another group of mice. Instead of gastric bypass, these mice had surgery that redirected bile acids to the latter part of the small intestine without altering the stomach.

Significantly, the team noted that this surgery also lowered primary bile acid levels in the bloodstream and decreased the size and spread of colorectal tumors as effectively as gastric bypass surgery. This was supported by an additional experiment, where they identified that primary bile acids promote the growth of colorectal cancer cells in laboratory settings.

The results indicate that focusing on primary bile acids may hold promise for cancer treatment. “We might be able to leverage various oral medications designed to reduce these bile acids to replicate some of the advantageous effects of gastric bypass surgery,” notes Vance Albaf from Louisiana State University.

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Source: www.newscientist.com

Cancer Cells Hijack Mitochondria from Neurons to Fuel Their Growth

Posted on June 25, 2025 by Igor Mitreski

Neurons Growing Among Cancer Cell Cultures (Stained Green)

Simon Grelet and Gustavo Ayala

Cancer cells are known to hijack energy-generating components from neurons, facilitating their spread to remote locations. This groundbreaking discovery may enhance treatments for the most aggressive tumors.

“This marks the first instance of mitochondrial transfer from nerves to cancer cells,” states Elizabeth Lepasky, who is not directly linked to the study conducted at the Roswell Park Comprehensive Cancer Center in Buffalo, New York. “This signifies a pivotal advancement in cancer neuroscience, a rapidly evolving field.”

Prior knowledge indicated that both intratumor and adjacent tumors produce proteins and electrical impulses that promote cancer growth and dissemination. “A higher density of nerves within tumors correlates with a poorer prognosis,” says Simone Grelet from the University of Southern Alabama.

Earlier investigations have demonstrated that brain tumor cells can absorb mitochondria (the energy-producing organelles) from non-neuronal brain cells. However, the potential for tumor cells to extract mitochondria from neurons remained unclear, according to Grelet.

To explore this, Grelet and his team genetically modified breast cancer cells derived from mice to contain red fluorescent molecules and combined them with mouse neurons that had mitochondria labeled with green pigments in laboratory conditions. Imaging revealed that cancer cells can seize mitochondria from neurons within a matter of hours.

“Cancer cells extend their membranes to absorb mitochondria from neurons,” explains Grelet. “It’s akin to a lineup of mitochondria filtering through a narrow passage, entering the cancer cells sequentially.”

To assess whether this phenomenon occurs in vivo, the researchers injected red breast cancer cells into the mammary glands of female mice to induce tumor growth. They also genetically engineered the surrounding nerves to carry green mitochondria. Approximately one month later, 2% of the cancer cells in these tumors had taken up mitochondria from neurons.

Conversely, 14% of tumor cells that metastasized to the brain exhibited neuronal-derived mitochondria. This suggests that cancer cells acquiring mitochondria from nerves have a significant advantage over other cancer types. Further tests indicate that these mitochondria contribute to greater resilience against the physical and chemical challenges encountered in the bloodstream.

“Cancer cells face numerous hurdles in their migration,” remarks Repasky. “They must escape the primary tumor, navigate barriers to blood vessels, exit the bloodstream, and secure sufficient oxygen and nutrients at secondary sites. By appropriating mitochondria, it appears cancer cells can endure this tumultuous journey,” she adds.

To determine if this process also occurs in humans, researchers examined tumor samples from eight women with metastatic breast cancer. They discovered that tumor cells from distant sites contained, on average, 17% more mitochondria compared to those from breast tumors, suggesting that similar mechanisms are at play in patients, according to Grelet.

Moreover, the team analyzed human prostate tumor samples and observed that cancer cells near nerves contained significantly more mitochondria than those situated further away. “I believe this represents a common mechanism utilized by various tumor types,” asserts team member Gustavo Ayala from the University of Texas Health Science Center in Houston.

The findings indicate that inhibiting mitochondrial transfer could potentially curtail the spread of the deadliest tumors. “We are optimistic that this is achievable, at least for certain tumor types,” Repasky suggests. Ayala mentions that they are working towards developing a drug to facilitate this approach.

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Source: www.newscientist.com

CAR T-Cell Therapy Can Be Administered to Cancer Patients

Posted on June 19, 2025 by Igor Mitreski

Illustration of CAR T-cell therapy targeting multiple myeloma, a type of blood cancer

Nemes Laszlo/Alamy

CAR T-cell therapy has the potential to transform cancer treatment. This innovative treatment genetically alters immune cells to combat diseases but is both complex and costly. Researchers have recently achieved the ability to develop personalized therapies within the bodies of non-human animals.

This form of treatment is primarily accessible in the UK and the US for select patients with various blood cancers, such as certain leukemias, where B cells—crucial immune components—grow uncontrollably. The process entails extracting T cells from a patient’s blood, genetically modifying them to target and destroy B cells, then duplicating and reintroducing these modified cells back into the patient’s body.

Nonetheless, this method is time-intensive. “You need to take the blood and send it to the Central Manufacturing Institute before it can be returned,” explains Carl June from the University of Pennsylvania. “This makes scaling the process challenging.” Additionally, the treatment comes at a steep price: over $500,000 per patient.

In search of a more efficient method, June and his team focused on gene molecules that deliver instructions to produce proteins that target B cells. They encapsulated these molecules in fat droplets, allowing entry into T cells, where they can identify and eliminate B cells. However, this effect is temporary, as the RNA code degrades within a week.

The researchers injected cancerous human B cells and healthy T cells into mice lacking an immune system. After a week, they administered five fat droplets to these mice over a span of two weeks, with some receiving higher doses.

Three weeks later, the mice that received the highest dose displayed no detectable tumor cells and no side effects. “The level of tumor cells was as minimal as we could measure,” remarks June.

The team also administered fat droplets to 22 healthy monkeys, resulting in the production of CAR T cells within their bodies and completely eradicating all B cells within just one day. Although B cells are essential for antibody production, the treatment was well tolerated by all but one monkey, which experienced a severe inflammatory response.

“This is truly remarkable,” says Karin Straathof from University College London. This could represent a significantly easier and more affordable method for implementing CAR T-cell therapy, she asserts.

However, one downside of standard CAR T-cell therapies is their ability to provide long-lasting protection, notes Straathof. The newly developed technique temporarily produces these cells; if cancer returns, additional treatments will be necessary. Furthermore, the effectiveness and safety of this approach in humans remain unverified, pending clinical trials.

June confirms that the team is currently testing the method in healthy humans. “The first patient was treated in the past few weeks,” he states.

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Source: www.newscientist.com

Researchers Utilize Enhanced DNA Techniques to Classify Breast Cancer

Posted on June 12, 2025 by Igor Mitreski

Triple-negative breast cancer (TNBC) is recognized as one of the more aggressive and challenging breast cancers to treat. Lacking the three standard hormonal markers associated with estrogen receptors, progesterone receptors, and HER2, this absence complicates the selection of effective treatment strategies for healthcare providers.

Researchers characterize TNBC as a collection of various diseases with distinct molecular characteristics that impact how the cancer manifests and its response to treatments. They utilize specific genes and gene products to categorize TNBC types. It is important to note that there are overlaps in the current classifications, which might be explained by the presence and levels of particular chemical molecules on the DNA. These molecules play a role in regulating whether genes are activated or deactivated in cells through processes known as DNA methylation.

In this study, researchers from Sweden explored how the distribution and patterns of DNA methylation delineate different forms of TNBC, influencing tumor behavior and interactions with the body’s immune system and its treatment responses. They analyzed 235 tumor samples from various patients in Sweden, ensuring that the data was refined to focus solely on cancerous cells rather than healthy tissue.

Employing a statistical technique known as Non-negative matrix factorization, they identified two primary categories of TNBC based on DNA methylation patterns: basal and nonbasal groups. This categorization aligns with previous classifications grounded in how cells interpret gene functions, termed gene expression. The basal group comprised tumors that were typically more active in immune responses and had a higher incidence of mutations linked to DNA repair issues, notably involving the common BRCA1 gene. Conversely, although the nonbasal group lacked hormone receptors, they exhibited increased activity in genes that influence hormonal responses.

Utilizing statistical assessments, the researchers subdivided each major group into smaller subtypes. Within the basal tumors, they identified three subgroups, referred to as basal1, basal2, and basal3, characterized by varying levels of immune cell activity and gene expression profiles. One specific subgroup, Basal3, demonstrated elevated expression of proteins that aid tumors in evading the immune system. The researchers found that specific DNA methylation patterns could activate or deactivate these proteins, indicating that patients with basal tumors might benefit from existing cancer treatments targeting this protein. The Basal2 subgroup expressed genes that inhibit immune activity, while the Basal1 subgroup displayed no significant immune-related behavior.

In the nonbasal category, researchers distinguished two subtypes: nonbasal1 and nonbasal2. Both of these subgroups were more prevalent among older patients and exhibited lower survival rates compared to the basal subgroup. The Nonbasal2 group encompassed tumors that influenced hormonal activity and responses to fatty treatments, whereas the Nonbasal1 group experienced more frequent disruptions in genes associated with tumor suppression.

Across all groups, researchers identified numerous genes whose methylation could modulate tumor growth and responses to the surrounding environment. To validate their findings in a broader context, they sourced independent tumor datasets from global databases and conducted similar classification analyses. They confirmed that the identified methylation subtypes appeared in other TNBC samples and correlated methylation patterns with tumor defense mechanisms, pinpointing strategies TNBC tumors may utilize to evade the immune system.

The researchers also acknowledged several limitations of their study. Their focus on DNA methylation represents just one of many chemical modifications that can influence TNBC behavior. Some of the independent datasets utilized originated from general breast cancer studies and were not exclusively focused on TNBC. Additionally, a significant portion of the data came from Western and Northern European populations, which may limit the applicability of the findings to individuals from other ethnicities. They emphasized the necessity for larger and more diverse datasets to gain a comprehensive understanding of TNBC subtypes.

In conclusion, the researchers posited that examining DNA methylation in patient samples could effectively categorize TNBC into meaningful subtypes, each with unique biological features, immune environments, and potential treatment responses. They recommended that future studies explore the origins of epigenetic modifications, such as DNA methylation, and how these alterations contribute to variations in TNBC subtypes.

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Source: sciworthy.com

New AI Tools Predict Which Men Will Respond to Prostate Cancer Treatments

Posted on May 30, 2025 by Igor Mitreski

Medical professionals have created an artificial intelligence tool capable of predicting which men diagnosed with prostate cancer are likely to benefit from treatment, potentially lowering the risk of mortality.

Abiraterone is regarded as a revolutionary treatment for the condition, which is the most prevalent cancer among men in over 100 countries. It has already enabled countless individuals with advanced prostate cancer to enjoy extended lifespans.

Nonetheless, some nations, including the UK, have ceased offering this “remarkable” medication to men whose cancer has not metastasized.

Currently, teams from the US, UK, and Switzerland are developing AI assessments that determine which men are likely to gain from Abiraterone. This “promising” advancement enhances the healthcare system to allocate medications more effectively to suitable candidates while allowing others to avoid unnecessary treatments.

The AI test was unveiled in Chicago at the annual conference of the American Society of Clinical Oncology, the largest cancer conference globally.

Nick James, a professor specializing in prostate and bladder cancer research at the London Cancer Institute, serves as a consultant clinical oncologist at the Royal Marsden NHS Foundation Trust, where he leads the development team.

“Abiraterone has already greatly enhanced the prognosis for hundreds of thousands of men with advanced prostate cancer,” James stated. “We recognize that for many men whose cancer hasn’t spread yet, it can have significant implications.

“However, the treatment comes with side effects and necessitates additional monitoring for potential issues such as hypertension or liver abnormalities. It is extremely valuable to identify those most likely to truly benefit, as it may slightly elevate the risks of diabetes and heart complications.

“This research indicates that those who respond optimally to abiraterone, as well as those who fare well with standard treatments alone, can decide between hormone therapy and radiation therapy.”

The AI tool examines tumor images and identifies features that may not be discernible to the naked eye. Prostate Cancer UK, the Medical Research Council, and arterial funded teams analyzed biopsy images from over 1,000 men exhibiting high-risk prostate cancer that had not metastasized.

AI analysis pinpointed 25% of the men in the study who were most likely to gain from Abiraterone. For these individuals, the medication halved the risk of mortality.

In the study, patients received a score indicating a positive or negative biomarker. This was then compared with outcomes. Among those with biomarker-positive tumors, the risk of death was reduced from 17% to 9% after five years for one in four men.

For patients with biomarker-negative tumors, Abiraterone decreased the risk of death from 7% to 4%. The research team indicated this result was neither statistically nor clinically significant, meaning these men are better off with standard treatment alone and can avoid unnecessary therapies.

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Professor Gert Attard, the research co-leader at UCL Cancer Institute, noted, “This study highlights that, within a sizable cohort of patients, new algorithms can be utilized to glean information from routinely available pathology slides to customize treatments to individual patients, thereby minimizing unnecessary interventions while maximizing the effectiveness of treatment.”

James mentioned that fewer men may require the medication than previously believed, suggesting that health services should contemplate administering it to men whose cancer hasn’t spread.

While it has been sanctioned for use within the NHS for advanced prostate cancer in England, it has yet to receive approval for newly diagnosed high-risk cases that have not metastasized. However, men with indications of high-risk cancer have had access to treatment in Scotland and Wales for two years.

“Abiraterone costs just £77 per pack compared to thousands for new treatments,” James remarked. “We sincerely hope this new research will clarify who truly benefits from this drug, especially given NHS England’s decision not to fund it for high-risk non-metastatic prostate cancer cases.”

Dr. Matthew Hobbs, research director at Prostate Cancer UK, termed the AI test as “promising.” He further elaborated:

Source: www.theguardian.com

Enhanced Cancer Screening Could Detect Early Cases in Women with Dense Breasts

Posted on May 22, 2025 by Igor Mitreski

High-density breast tissue and tumors resemble each other on scans.

Golodenkov/Shutterstock

Recent research indicates that those with dense breast tissue may gain from an additional round of cancer screening, as a significant trial uncovered tumors that were overlooked in standard mammograms.

In the UK, mammograms—an x-ray scan used for breast cancer screening—are provided for individuals aged 50 to 71. These scans look for white spots that indicate cancer presence. However, around 50% of women in this age range have dense breasts, characterized by a high amount of fibrous and glandular tissue, also appearing white on the scans. This similarity complicates tumor detection.

“The challenge with dense breasts is that cancers may go unnoticed until they grow significantly large, which negatively affects prognosis,” said Thomas Hervich, who wasn’t a part of the study at the Medical University of Vienna in Austria.

To determine whether additional screenings can help, Sarah Vinnicombe and her colleagues at the University of Dundee recruited over 6,000 women aged 50-70 from across the UK. Participants were randomly divided into three groups, each receiving extra screening through advanced x-ray methods such as MRI, ultrasound, or contrast-enhanced mammography.

In this extended screening phase, MRI and contrast-enhanced mammography together identified 85 small tumors—three times as many as detected by ultrasound. Twelve of these tumors were located in milk ducts, suggesting a lower likelihood of spreading beyond the breast. Conversely, the other 73 tumors were invasive, increasing the risk that cancer could migrate into surrounding breast tissue and beyond.

“Detecting these cancers is crucial. They typically grow over time, and finding them within three to four years can lead to larger sizes,” stated Hervich. “Some tumors are aggressive, so I believe supplemental screening could save lives.”

However, it’s uncertain if this will hold true. For instance, a 2021 trial on ovarian cancer screening revealed a decrease in cases but did not correlate with increased longevity. Additionally, some tumors detected may not be cancerous or aggressive. Thus, unnecessary screening could lead to undue anxiety and treatment.

The researchers plan to continue monitoring participants to assess whether supplementary screenings result in saved lives.

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Source: www.newscientist.com

Factors That Truly Influence Your Prostate Cancer Risk

Posted on May 21, 2025 by Igor Mitreski

Prostate cancer is the most prevalent cancer among men, with roughly one in eight men receiving a diagnosis in their lifetime. Nevertheless, not all prostate cancers are life-threatening; in fact, many develop slowly and remain harmless.

“There are essentially two categories of prostate cancer,” Dr. Haley Luxton, who studies the impact of prostate cancer in the UK, explains. “I refer to them as ‘pussycats’ and ‘tigers.’ Pussycats are the slow-growing types, which typically do not lead to death.”

“On the other hand, tigers are highly aggressive forms of prostate cancer, and these men require immediate treatment to prevent mortality.”

Autopsy research indicates that over 50% of men over 90 have prostate cancer cells, many of whom were never diagnosed during their lifetime.

“Most men will eventually have prostate cancer cells,” adds Dr. Cody Watling, a postdoctoral researcher at the National Cancer Institute. “However, whether it becomes clinically significant—causing symptoms or spreading—is an entirely different issue.”

Three Key Risk Factors

What really increases your risk of prostate cancer?

According to science, there are three major factors—sadly beyond your control:

Age – The risk increases significantly after age 50, with most diagnoses occurring in men over 70.
Ethnicity – Black men are twice as likely to develop prostate cancer as their white counterparts. The reasons remain unclear, although genetics may play a role.
Family History – If your father, brother, or grandfather had prostate cancer, your risk is elevated—especially if the diagnosis occurred before age 60. The BRCA2 gene is a contributing factor.

Watling notes that these risk variables are generally linked with both prostate cancer and more aggressive forms of the disease. “Evidence suggests that age, family history, and being Black increase the overall risk of aggressive prostate cancer.”

More than 50% of men over 90 have prostate cancer cells, but many are benign. – Getty

Lifestyle Considerations

While some reports suggest that lifestyle choices can reduce risk, the situation is complex.

Watling, who researched diet and prostate cancer risk at Oxford University, stated, “To date, strong evidence has been elusive.”

Some studies indicate a potential link between high consumption of dairy, particularly milk, and slight increases in prostate cancer risk, likely due to a growth factor known as IGF-1. However, Watling emphasized, “The evidence remains ambiguous, and there is no robust connection.” More research is necessary to clarify these relationships.

One possible exception is obesity. “There is some evidence suggesting that being overweight correlates with a higher risk of aggressive or fatal prostate cancer,” says Watling. “However, it’s challenging to determine if this is biological or due to less frequent early screening in heavier individuals.”

Luxton concurs: “Maintaining a healthy, balanced diet and engaging in some form of physical activity—even just a ten-minute walk—can be beneficial.”

Recommendations

If you are over 50, or over 45 with a higher risk (due to family history or being Black), Prostate Cancer UK advises initiating a conversation with your GP.

You can assess your risk in just one minute with the Prostate Cancer UK Online Risk Checker.

Your doctor may then conduct various screening tests, including prostate-specific antigen (PSA) blood tests, examinations, and MRI scans as necessary.

In Conclusion

Joe Biden’s diagnosis understandably alarmed many, but it also led to a surge of misleading or overly simplistic guidance. Here are the facts:

The risk of prostate cancer cannot be entirely eliminated.
Most risks are linked to age, family history, and ethnicity, rather than diet or lifestyle factors.
Nevertheless, healthy habits remain important for reducing the risk of aggressive prostate cancer and other diseases.
If you are at high risk, it’s crucial to speak with your doctor.

About Our Experts

Hailey Luxton is the Head of Research Impact and Engagement at Prostate Cancer UK, tasked with identifying initiatives that can significantly influence the charity’s research program and expedite research projects. Previously, he conducted research at University College London and Cancer Research UK.

Cody Watling is a postdoctoral researcher at the National Cancer Institute. His research has been featured in publications such as BMC Medicine, Clinical Nutrition, and British Journal of Cancer.

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Source: www.sciencefocus.com

Here’s what we often misunderstand about prostate cancer.

Posted on May 20, 2025 by Igor Mitreski

Joe Biden’s recent prostate cancer diagnosis has brought awareness to these health issues within the public discourse.

Prostate cancer charities are urging men across the country to assess their cancer risk through signs and to seek medical advice if they experience symptoms like frequent and uncontrollable urination. Nevertheless, prostate cancer remains a nuanced and intricate condition.

The prostate gland is located beneath the bladder and typically enlarges with age. The urethra, which drains urine from the bladder, passes through the prostate. Consequently, when the prostate enlarges, it can compress the urethra, impeding urine flow and leading to symptoms such as dribbling and increased urgency to urinate. Overall, this is a prevalent condition.

Likewise, the incidence of cancers originating in the prostate is quite common. Autopsy studies indicate that 36% of white individuals and 51% of African Americans had unreported prostate cancer. In the 1970s, he was diagnosed with prostate cancer.

Photo credit: Getty

Another study suggested that five percent of men under 30 lived with prostate cancer. This may seem surprising, but these cancers were identified during autopsies of men who passed away from other causes. Medical professionals have long maintained certain sayings, such as “That’s how I die from prostate cancer.”

This presents a significant challenge concerning prostate cancer. It can manifest in a form that causes minimal harm while also possessing a variant that is potentially lethal and can metastasize to nearby organs and bones.

How Dangerous Is Prostate Cancer?

Currently, prostate cancer accounts for approximately 35,000 deaths in the U.S. each year, with over 313,000 men diagnosed annually.

The key to addressing this issue lies in identifying which cases pose a threat, as treatments like surgery, radiation therapy, and hormone therapy may have side effects such as long-term erectile dysfunction and incontinence.

It is essential that patients avoid unnecessary treatments that do not benefit them.

Unfortunately, there is currently no straightforward method to differentiate between aggressive tumors and those that are indolent. A blood test known as the PSA (prostate-specific antigen) test was created in the 1990s to monitor men’s responses to prostate cancer treatments.

Following its introduction, the number of diagnosed prostate cancer cases surged, yet there was no corresponding decrease in mortality rates.

This led Richard Alvin, the researcher who developed the PSA test, to remark, “The widespread use has resulted in a costly public health crisis.” This is due to the PSA test potentially generating false positives caused by factors aside from prostate cancer, including infections and benign prostate enlargement.

In the U.S., the Preventive Services Task Force reviews research independently and issues recommendations regarding screening.

They state that PSA screening can marginally lower the risk of death from prostate cancer in some men. However, many men may experience harm from the screening, including false positives leading to unnecessary tests and diagnoses of non-threatening issues.

In short, increased screening rates in the U.S. may have contributed to deteriorating health outcomes for men, as they pursued treatments for conditions detected through positive test results that were not life-threatening.

Despite a reduction in testing rates since their peak in the ’90s, prostate cancer mortality rates in the U.S. have gradually decreased over the years. This might be attributed to improved treatment protocols, rather than indicating benign prostate enlargement. Limiting trials to men who exhibit symptoms of prostate enlargement could prevent unnecessary cancer treatments.

In other regions, such as in Sweden, prostate cancer screening cut mortality rates from 1.7% to 0.98%, although this required diagnosing 13 men to prevent a single death.

What is the Solution?

To mitigate this issue and avoid unnecessary treatments, a “watchful waiting” approach has shown efficacy. A recent 15-year British study indicated that localized prostate cancer with low mortality rates whether treatment included radiation, prostate removal, hormone therapy, or observation. This underscores the futility of invasive treatments offering no significant benefits.

So, what steps can we take? In the UK, the National Screening Committee regularly reviews the recommendation for PSA screening for prostate cancer. Recent research has identified harmful cancers through MRI screenings, but there is still insufficient evidence regarding whether this can reduce death rates while minimizing excessive treatments.

Meanwhile, straightforward messages regarding the benefits of screening are being communicated to men without adequately addressing the potential drawbacks. Numerous screening events are organized by well-meaning charities during sports events. Advocates argue that informed consent is critical; otherwise, we risk offering false promises and ensuring minimal progress in men’s health.

This article was published in 2024

Read more:

Source: www.sciencefocus.com

Doctors say Biden’s prostate cancer diagnosis is unusual, but not unprecedented.

Posted on May 20, 2025 by Igor Mitreski

New information regarding former President Joe Biden’s prostate cancer diagnosis indicates that while his case is not common, it is not entirely unheard of, according to the healthcare professionals who treated him.

At 82, Biden received a diagnosis of aggressive cancer on Friday after a nodule was found in his prostate, his personal staff announced. The cancer has spread to his bones, but his office stated that he is likely to respond well to treatment.

Most prostate cancer diagnoses occur at an early stage through routine screenings, which may include blood tests or rectal exams.

However, approximately 8% of cases have already metastasized to other organs by the time of diagnosis. In such instances, oncologists believe the patient may have had prostate cancer for several years, possibly up to a decade.

“We’ve encountered numerous patients facing significant health challenges,” stated Dr. William Dahoot, chief science officer at the American Cancer Society.

That said, exceptions exist.

“While most prostate cancers are slow-growing, some can develop rapidly and pose a high risk of metastasis,” explained Dr. Aron Weiser, a urologist and chief medical officer. “Is it common? No. But it can occur, dependent on the unique biology of that cancer.”

Screening facilitates early detection, yet there is disagreement among healthcare professionals regarding who should be screened for prostate cancer.

Many physicians refrain from screening men in their late 70s or 80s, as these individuals are generally more likely to die from other medical issues than prostate cancer. Nevertheless, with increasing life expectancies, some doctors consider screening appropriate for healthier older men.

According to the American Cancer Society’s recommendations, men in their 50s and 60s should be screened every two years. Men with elevated levels of prostate-specific antigens—a protein made by the prostate—should undergo annual screenings. Additionally, men at higher risk for prostate cancer, such as African Americans or those with a family history of the disease, should begin screening in their 40s.

However, current guidelines from the U.S. Task Force on Preventive Services, an independent panel that advises on practices often covered by insurance, state that men aged 55 to 69 should only consider discussing blood tests with their physicians. The task force is currently reviewing new screening guidelines for prostate cancer, with many healthcare providers advocating for a broader recommendation.

Weiser noted that there was a broader screening approach in the late 1980s and early 1990s, leading to premature diagnoses and treatments that may not have impacted patients’ lives. The 2012-2018 U.S. Preventive Services Task Force recommended blood tests to help identify prostate cancer, resulting in decreased screening rates.

“Prostate cancer behaves differently; many cases are benign, not causing issues for individuals,” Weiser remarked. “The goal should be to identify aggressive cancers.”

In recent years, there has been a shift back toward increased screening as doctors have improved their understanding of which cases require treatment versus those that should be monitored.

Nevertheless, Dahut expressed ongoing concerns among patients and physicians about whether the benefits of screening outweigh the risks of overdiagnosis and overtreatment. Screening rates have declined steadily since 2012, and Dahut notes that this trend has led to a 5% increase in diagnoses of more advanced prostate cancer.

It remains unclear whether Biden has undergone prostate cancer screenings in recent years. His annual physical examination in February 2024 did not indicate a screening was performed, which is not unusual for someone of his age. A physical exam in 2019 revealed an enlarged prostate but did not lead to a cancer diagnosis at that time.

Dr. David Shusterman, a urologist based in New York, stated that Biden’s advanced diagnosis is atypical among patients who are screened regularly.

“It is rare for metastasis to have occurred in someone who regularly sees a urologist,” he said.

Diagnosis is often more prevalent in individuals who do not maintain regular medical consultations. Rick Gum is one such case; he was never screened before his prostate cancer diagnosis in 2018. Gum, a 73-year-old trucking company owner from Big Rock, Illinois, initially sought care for a hernia but was found to have aggressive cancer that had spread to his bones.

“I learned the hard way,” he remarked. “I should have visited the doctor.”

Gum noted that his cancer was too advanced for standard treatment, prompting his participation in various clinical trials at Northwest Medicine, which included chemotherapy, radiotherapy, and treatments involving radioisotopes.

“I’ve enjoyed seven excellent years since my diagnosis,” he reflected. “They’ve been quality years. I ride motorcycles, travel a bit, and love my work. I’ve been able to do it all.”

According to the American Cancer Society, around 37% of patients with metastatic prostate cancer survive at least five years post-diagnosis.

Dr. Peter Nelson, vice president of precision oncology at the Fred Hutch Cancer Center, mentioned that patients like Biden could have over a 90% response rate to treatments that lower testosterone—a hormone that can promote cancer growth. These hormonal therapies are typically administered through injections or tablets.

“He may start with multiple medications and anticipate several years of effective treatment before any resistance develops,” Nelson noted. Some patients also receive chemotherapy or radiation in conjunction with hormone therapy, he added.

According to sources familiar with the family’s perspective, Biden and his family are exploring “multiple treatment options,” including hormone therapy.

Source: www.nbcnews.com

Approach to Prostate Cancer Diagnosis: Insights from Biden’s Patient Care Strategies

Posted on May 19, 2025 by Igor Mitreski

Prostate cancer specialists assert that former President Joseph R. Biden’s diagnosis is grave. Announced by his team on Sunday, it was revealed that the cancer has metastasized to his bones and is classified as Stage 4, the most severe stage of the illness. This condition is currently incurable.

However, prostate cancer professionals highlight that advancements in the diagnosis and treatment of prostate cancer have significantly improved the outlook for men facing advanced disease, primarily based on research funded by the National Institutes of Health and the Department of Defense.

“We’ve explored numerous avenues for intervention,” remarked Daniel W. Lynn, a prostate cancer specialist at the University of Washington.

Dr. Judd Mull, a prostate cancer expert at Duke University, noted that men experiencing prostate cancer that has spread to the bones can now “survive five, seven, ten years or even longer” with current treatments. In the 1980s, men like Biden might “wish to pass away from natural causes rather than from prostate cancer,” he pointed out.

Biden’s office indicated that he experienced urinary symptoms, which prompted him to seek medical evaluation.

However, Dr. Lin expressed skepticism, stating, “I don’t believe his symptoms were related to the cancer.”

Instead, he suggested that the most plausible sequence was that doctors had examined Biden, discovered a nodule in his prostate, and conducted blood tests and prostate-specific antigen tests. PSA tests detect proteins produced by cancer cells and can follow blood tests and MRIs that indicate cancer.

Currently, Biden and other patients diagnosed with metastatic prostate cancer are in a better situation than past patients. There are approximately ten novel treatments available for the disease that have significantly altered the prognosis.

The primary strategy is to inhibit the testosterone that fuels prostate cancer. When Dr. Muru began his practice as a urologist in the 1980s, this was achieved by surgically removing the testicles. Today, men have the option of two medications administered via injection that prevent testosterone production, alongside oral pills that achieve the same result.

However, these medications alone are insufficient. Therefore, physicians typically add one of several androgen blockers that further suppress testosterone.

Some men receive supplementary treatments such as chemotherapy or radiation, depending on the extent to which the cancer might spread within the bones.

There have also been advancements in diagnostic procedures.

Previously, doctors assessed the degree of cancer in the bones through scans that detected inflammation. Now, they utilize a more precise scan known as the Prostate-Specific Membrane Antigen (PSMA) PET scan. This scan employs a radioactive tracer that binds to markers on the surface of prostate cells, allowing for faster cancer detection. Consequently, men with prostate cancer cells in their bones now often have a considerably better prognosis compared to those who underwent bone scans just a few years ago.

Additionally, there are medications available that block testosterone and others that can target cancer if chemotherapy and radiation therapy become ineffective.

Dr. Lynn pointed out that increased federal research funding, alongside Biden’s initiative to prioritize cancer research, has contributed to these advancements. He noted that Biden was “one of the first presidents to elevate cancer awareness.”

Regarding Dr. Muru, he remarked that men who develop stage 4 prostate cancer are now often filled with a sense of hope.

“There are now even more resources at our disposal,” Dr. Moul added. “The survival rate has nearly tripled in the last decade. The extent of change is truly remarkable.”

Source: www.nytimes.com

Immunotherapy Drugs: A Hopeful Alternative to Invasive Surgeries and Strenuous Treatments for Cancer Patients

Posted on April 27, 2025 by Igor Mitreski

When individuals develop solid tumors in the stomach, esophagus, or rectum, oncologists have established treatment strategies. Yet, these treatments can significantly affect quality of life, leading to outcomes such as stomach and bladder removal, permanent colostomy bags, radiation exposure, infertility from chemotherapy, and lasting bodily harm.

In response, a research team at Memorial Sloan Kettering Cancer Center utilized drugs from GSK to explore a novel approach.

They initiated the study with 103 participants, who represent a small fraction (2-3%) of cancer patients with tumors ideally suited for immunotherapy—drugs designed to bypass obstacles that prevent the immune system from attacking cancer cells.

Notably, clinical trials do not generally expect immunotherapy to replace standard treatments. Researchers, led by Dr. Lewis A. Diaz Jr. and Andrea Cerseck, opted to administer dostarlimab, an immunotherapeutic agent.

The outcomes were unexpected and offered hope for a select group of patients faced with these cancers.

In 49 patients with rectal cancer, tumors vanished and did not return after five years. Among 54 patients with other cancers—including esophageal, liver, endometrial, urinary tract, and prostate cancers—35 experienced total tumor disappearance.

Out of the 103 patients, only five experienced a recurrence of cancer. Three were given three doses of immunotherapy, while one was discontinued after the tumor reappeared in the lymph nodes. Currently, the four patients show no signs of disease, while the fifth received further immunotherapy to reduce the tumor size.

On Sunday, investigators presented their findings at the American Cancer Research Association’s Annual Meeting, with a paper featured in the New England Journal of Medicine.

Dr. Bert Vogelstein, an oncologist at Johns Hopkins in Baltimore, termed the results “groundbreaking.”

The drug development’s early stages were conducted in his lab, where he expressed surprise at the advancements.

“The concept of treating large tumors from various organs without surgery seemed like science fiction 20 or 30 years ago,” he noted. However, he emphasized that these discoveries stemmed from decades of foundational research.

The reason immunotherapy succeeded for these significant tumors lies in their gene incompatible repair mutations, which obstruct the correction of DNA damage. This leads to tumors accumulating abnormal proteins that signal the immune system for destruction. Nevertheless, the tumors deploy a shield to fend off immune attacks, which immunotherapy can stimulate, enabling the immune system to target the tumors effectively.

For patients like those in this study, Dr. Michael Oberman, a gastrointestinal cancer specialist at MD Anderson Cancer Center in Houston, suggests the results point towards immunotherapy as an option free of chemotherapy, radiation, or surgery.

However, obstacles remain. The drug is priced around $11,000 per dose, requiring patients to undergo nine infusions over six months. To qualify for insurance coverage, it needs inclusion in clinical guidelines established by professional organizations.

The drug is approved for treating uterine cancer with mismatch repair mutations and is also listed in clinical guidelines for rectal cancer, based on previous small-scale studies. Yet, Dr. Diaz indicated that other cancer patients may face challenges in taking the medication. Nonetheless, Memorial Sloan Kettering continues to recruit participants for clinical trials, meaning those with eligible tumors can access the drug at no cost.

For some individuals, immunotherapy is life-transforming. Side effects can occur, with the study noting fatigue, rashes, and itching as the most common. Rare side effects included pulmonary infections and encephalitis.

Maureen Sidris, a 71-year-old from Amenia, New York, discovered she had cancer after struggling to eat a burger.

“It wouldn’t go down,” she recounted, realizing there was some blockage. Ultimately, it was identified as a tumor at the junction of her stomach and esophagus.

In 2019, she visited Sloan Kettering, where her surgeon advised that surgery, chemotherapy, and radiation were mandatory and that surgery would be complex.

However, due to her tumor’s mismatch repair mutation, she was able to join a clinical trial. Her first injection occurred on October 14 of that year, and by January, her tumor had disappeared. While Sidris experienced one side effect from the treatment requiring medication to support her kidney function, she considers it worthwhile to avoid the challenging treatments initially suggested.

“It was indeed a journey,” she remarked. However, she reasoned that she had everything to gain and nothing to lose by trying immunotherapy.

“If it didn’t succeed, I still had surgery as a backup,” she concluded.

Source: www.nytimes.com

ICE detains Harvard scientists analyzing images that could alter cancer diagnosis

Posted on April 22, 2025 by Igor Mitreski

Harvard Medical School’s cutting-edge microscopes have the potential to revolutionize cancer detection and lifespan research. However, a scientist who developed computer scripts to extract maximum information from the images found herself in immigration detention for two months, jeopardizing significant scientific advancements.

The scientist in question is 30-year-old Russian-born Xenia Petrova, who worked at Harvard’s renowned Kirschner Institute until her arrest at Boston Airport in mid-February. Currently detained at the Richwood Correctional Center in Monroe, Louisiana, Petrova is fighting against deportation to Russia, where she fears persecution and imprisonment due to her participation in protests against the conflict in Ukraine.

The incident involving Petrova and the detention of scholars across the country have hindered American universities’ ability to attract and retain crucial talent, a concern raised by Petrova’s colleagues. In fields where expertise is highly specialized, the loss of talent could have grave global implications for the future of medicine and scientific discovery. Scientists and faculty members are contemplating leaving institutions nationwide out of fear that their visas may be revoked or impacted by immigration enforcement actions.

“It’s like a meat grinder,” Petrova, as per a person talking to NBC News from the Louisiana facility, described her situation. “We are all in this system, regardless of having a visa, green card, or a valid reason.”

Petrova’s first immigration court hearing in Louisiana is scheduled for Tuesday morning, where she expects more clarity on her asylum case. Dr. Leon Peshkin, a prominent research scientist at Harvard University’s Faculty of Systems Biology and Petrova’s supervisor, received a call from Customs and Border Protection on February 16, notifying him of Petrova’s detention at Logan International Airport for failing to declare a sample of frog embryos used in research.

International researchers are increasingly anxious about the Trump administration’s strict stance on illegal immigration, with concerns that these policies could deter other foreign scientists from coming to Harvard. Recent surveys indicate a significant portion of scientists are contemplating relocating to Europe or Canada due to actions taken by President Donald Trump.

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Surprising increase in colorectal cancer diagnoses among individuals under 50

Posted on March 4, 2025 by Igor Mitreski

Immediately after my 54th birthday, I received the package. The enclosed instructions said the next time I empty my intestines, I should shave a little of the stool, shave it into a small sample bottle, seal it in a prepaid envelope and drop it in a post. I did the act and a few weeks later I was invited to the hospital. My sample contained blood. Colonoscopy was ordered to rule out colorectal cancer.

Thankfully, I don’t have colorectal cancer. Colonoscopy of 54 is not a classic start to middle age. However, over the next few years, this particular rite of passage may begin to occur much earlier. The proportion of this cancer among people in my age group has been declining thanks to screening programs like this, but talking about under 50 years is much more troubling.

Early onset colorectal cancer (EOCRC) is now the circumstance, as is known in people under the age of 50, due to its virtually unprecedented nature of the 20th century. 10% of all new cases worldwide. That number is expected to more than double by 2030, and by then EOCRC is expected to be the most common form of fatal cancer among Americans aged 20-49.

The reasons are uncertain, but ambitious new projects explore potential causes. The idea is that EORC may also be a more clear and aggressive form of illness. Meanwhile, as routine screening expanded to younger groups – in January, the UK reduced the screening age to 50 – and the new, less invasive test…

Source: www.newscientist.com

Big animals face heightened cancer risk, yet enhanced defenses have emerged

Posted on February 25, 2025 by Igor Mitreski

African elephants have extra copies of genes that help resist cancer

Neil Aldridge/Nature Picture Library/Aramie

Larger animals live longer and have more cells, and are expected to be at a higher risk of developing cancer. A comprehensive analysis of 263 species suggests that this is true, but also finds that some large animals have evolved ways of reducing risk.

“We provide the first empirical evidence that there is a link between body size and cancer prevalence, meaning that larger species increase cancer than smaller species. “I say it. George Butler University College London.

The results are in contrast to previous studies found. There is no link between weight and cancer rate. But many of these were related to just a few dozen species, Butler says.

To gain a broader view, Butler and his colleagues analyzed data on the size and cancer rates of 79 bird species, 90 mammal species, 63 reptiles and 31 amphibians. The data comes from previous studies by other researchers who sifted through autopsy records that record whether a breeding animal stored in a place like Zoos or an aquarium had cancer when it died. .

The team found that smaller animals were slightly more likely to have cancer than fewer animals at the time of death. Each 1% increase in body weight was associated with an average increase of 0.1% in cancer rates between birds and mammals. Because body mass data were not available in reptiles and amphibians, the team used body length and found that it was associated with an average increase in cancer rate of 0.003% for every 1% increase.

Butler and his team say their discoveries will challenge a long-standing idea known as the Pete Paradox. on the other hand, Veragolbunova At the University of Rochester in New York, the weak correlation still needs explanation.

“The increased risk they see is very, very minor and not proportional to their body size,” she says. “If you take small animals like mice and humans are 100 times larger, or elephants are 100 times larger, the difference in cancer rates is not 100 times higher in humans and 1000 times higher in elephants.”

It suggests that larger species have evolved more ways to protect themselves, Golbunova says.

Indeed, by using evolutionary trees to infer evolutionary rates of animal body size, the team said that if the size increases more rapidly during evolution, birds and mammal species of similar sizes can be We found it to provide better protection against cancer.

Previous studies have identified genetic adaptations in elephants and whales, protecting against cancer by improving DNA repair and preventing broken cells from dividing.

A deeper understanding of how some animals resist cancer can lead to new treatments for people, says Golbunova. “In these cancer-resistant animals, there are specific biological pathways of different fine-tuning, for example, targeting these pathways and then killing cancer cells more efficiently, or perhaps killing cancer cells. You can even prevent cancer from occurring,” she says.

“As these mechanisms have been tested over millions of years in the course of evolution, they are likely to become highly promising drugs,” she says.

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Source: www.newscientist.com

Early trials suggest mRNA vaccines hold potential for treating pancreatic cancer

Posted on February 20, 2025 by Igor Mitreski

Personalized mRNA vaccines, including those for pancreatic cancer treatment, are currently in phase 1 of clinical trials. The research was recently published in Nature.

Pancreatic cancer has one of the lowest survival rates among cancer types, with less than 13% of patients surviving beyond five years after diagnosis. The disease is often diagnosed at an advanced stage, with nearly 90% of cases already progressing when detected.

Pancreatic cancer cells have a high tendency to spread rapidly to other parts of the body, usually after the primary tumor has grown large. Symptoms typically only appear in late stages, and there are currently no routine screening methods like mammograms or colonoscopies for this cancer.

Effective treatments for pancreatic cancer are limited, with survival rates remaining around 10% despite the best available therapies. The development of personalized mRNA vaccines for cancer treatment aims to change this narrative.

Before the widespread use of mRNA vaccines for Covid-19, researchers were exploring their potential for cancer treatment. These vaccines work by training the immune system to identify and attack cancer cells, essentially turning the body’s immune response into a cancer-fighting mechanism. Current research is focused on melanoma, colorectal cancer, and other solid tumors.

The success of mRNA cancer vaccines relies on generating a robust response from T cells, a type of immune cell that recognizes and fights off intruders. These T cells need to be durable and capable of detecting and eliminating cancer cells, including those in pancreatic cancer which present unique challenges due to limited mutation targets.

A recent clinical trial evaluated the efficacy of an mRNA vaccine in pancreatic cancer patients who had undergone surgery to remove the tumor. Results showed that the vaccine elicited a response in half of the participants, generating tumor-targeting T cells that persisted for years. This promising outcome underscores the potential of mRNA vaccines in improving outcomes for pancreatic cancer patients.

The study also highlighted the need for further research to determine the long-term impact of these vaccines on patient outcomes. The development of ready-made mRNA vaccines that target common mutations in pancreatic cancer tumors is another area of ongoing investigation, offering a more standardized approach to treatment.

Overall, early findings suggest that mRNA vaccines hold promise in enhancing the body’s immune response against pancreatic cancer, offering hope for improved survival rates and outcomes in the future.

Source: www.nbcnews.com