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You are at:Home » Obesity directly correlated with increased risk of breast cancer, say researchers
Obesity Directly Correlated With Increased Risk Of Breast Cancer, Say
Science April 18, 2024

Obesity directly correlated with increased risk of breast cancer, say researchers

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Breast cancer affects thousands of people each year. Scientists have shown that many factors can influence breast cancer, including age, physical inactivity, and obesity. However, it is unclear exactly how obesity and breast cancer are related.

Previous researchers have shown that tissue inflammation in obese patients is related to cancer. Other researchers have shown that obese patients have the following characteristics: specific genetic mutations It is also related to cancer. However, how this mutation acts to generate different types of tumors is not fully understood.

Ha-Linh Nguyen and colleagues recently investigated the relationship between breast cancer and obesity. Nguyen and his team wanted to determine how obesity affects breast cancer by examining the tissue cell and genetic profiles of breast cancer in obese patients. Their goal was to see if doctors could develop more targeted treatments for breast cancer based on the genetic mutations involved.

They collected genetic data from the tumors of more than 2,000 breast cancer patients collected during multiple large-scale breast cancer studies conducted by five accredited cancer research institutions. To ensure that no changes had occurred in the breast tumors, the researchers only used data from patients who had not yet started cancer treatment.

The researchers defined obesity based on the patient’s weight-to-height ratio. body mass index, or BMI. They used patients’ BMI data to classify patients into three categories: obese, overweight, and underweight. An obese patient, her BMI was over 30 kilograms per square meter (kg/m2).2), the BMI of overweight patients was 25–30 kg/m2.2lean patients had a BMI of 18.5 to 25 kg/m.2. For reference, the average BMI for adults is approximately 26 kg/m3.2.

Patients were then further categorized based on breast tumor type. These categories include patients with tumors that originate in the milk-producing glands of the breast. Invasive lobular carcinoma tumoror a comparison of patients with ILC tumors and patients without specific tumor types.

The researchers also took into account other biological factors used to identify the type of breast cancer. estrogen receptor. Tumors in patients with estrogen receptor-positive breast cancer contain receptors that use the hormone estrogen to stimulate tumor cell growth. The tumors of breast cancer patients who are estrogen receptor-negative do not contain this receptor.

They also looked at another way to determine the type of tumor, a method called. HER2 factor. HER2-positive breast cancer patients contain a protein called human epidermal growth factor 2, which allows cancer cells to multiply rapidly. The researchers used these biochemical markers to classify patients by tumor type, and then used statistical analysis to distinguish between tumor types in obese patients and those in lean and overweight groups. We compared the types.

Researchers found that in obese patients with non-specific tumors that are estrogen receptor positive and HER2 negative, BMI influences breast cancer in the same way that age influences cancer development. The researchers explained that as we age, the body’s immune response slows down, giving cancer cells more time to accumulate before the body reacts and stops the process. They suggested that these results support the idea that both age and obesity are risk factors for developing breast cancer.

The scientists then looked at whether the tumors in each group had one or more cancer-causing mutations. The research team specifically looked at genes that researchers had previously shown had mutations that cause breast cancer. They also examined tumor DNA to see if there were mutations that caused deletions or amplifications of specific parts of the DNA. Change number of copies.

Researchers found different genetic mutations in patients with different BMIs. They found that a gene involved in cell division signaling, called P1K3CA, was less mutated in obese patients who were estrogen receptor positive, HER2 negative, and had unspecific tumors. Mutations in two other HER genes, CCND1 and CCNE1, were more common in obese patients with estrogen receptor-positive tumors.

The researchers concluded that their study showed a genetic link between breast cancer and obesity. They suggested that some genetic mutations found in tumors of obese patients, particularly CCND1 and CCNE1 mutations, may enable targeted breast cancer treatments. They suggested that future researchers should investigate how the biochemical pathways these genes are associated with actually contribute to breast cancer formation to better develop treatments. .


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original research: Obesity-related changes in the molecular biology of primary breast cancer

research has been published:July 21, 2023

research author: Harinh Nguyen, Tatiana Geukens, Marion Mehtens, Samuel Aparicio, Ayse Bassez, Ake Borg, Jane Block, Anejan Brooks, Carlos Caldas, Fatima Cardoso, Maxim de Schepper, Mauro DeLorenzi. , Caroline A. Drucker, Anuska M. Glass, Andrew R. Green, Edoardo Isnardi, Jörn Eifjords, Hazem Kout, Stian Knapskog, Savitri Krishnamurthy, Sunil R. Lakhani, Anita Langerod, John W. M. Martens, Amy E. McCart-Reid, Lee Murphy, Stefan Nauraz, Selina Nick-Zinal, Ines Nebelsteen, Patrick Neven, Martine Picard, Coralie Ponsetto, Kevin Puni, Colin Purdy, Emad A. Raka, Andrea Richardson, Emile Rutgers, Anne Vincent-Salomon, Peter T. Simpson, Marjanka K. Schmidt, Christos Sotiriou, Paul N. Spann, Kiat. Tee Benita Tan, Alastair Thompson, Stefania Tommasi, Karen van Baeren, Marc van de Wivel, Steven van Leer, Laura van't Veer, Giuseppe Viale, Alan Viali, Hanne Voss, Anke T. Witteveen, Hans Wildyas, Giuseppe Floris, Abhishek D. Garg, Anne Smeets, Dieter Lambrecht, Elia Biganzoli, Francois Richard, Christine Desmet

The research was conducted at the following locations:: Katholieke Universiteit Leuven (Belgium), Lund University (Sweden), Netherlands Cancer Institute (Netherlands), University of Cambridge (UK), Champalimaud Clinical Center/Champalimaud Foundation (Portugal), University of Lausanne (Switzerland), SIB Swiss Institute of Bioinformatics (Switzerland), Antoni van Leeuwenhoek Hospital (Netherlands), University of Nottingham (UK), University of Iceland (Iceland), University Hospitals of Leicester NHS Trust (UK), University of Bergen (Norway), and University of Texas MD Anderson. University of Queensland, Herston (Australia), Royal Brisbane and Women's Hospital, Herston (Australia), Oslo University Hospital, Ullenjausen (Norway), Erasmus University Medical Center, Rotterdam (Netherlands), University of Manitoba , Manitoba Institute for Cancer Treatment (Canada), University Hospital Leuven (Belgium), Jules Bordet Institute and Free University of Bruxelles (Belgium), European Organization for Research and Treatment of Cancer (EORTC) Headquarters (Belgium), University of Dundee (UK) , Nottingham University Hospitals NHS Trust (UK), Johns Hopkins University (USA), Netherlands Cancer Institute (Netherlands), Institut Curie, PSL Research University (France), Radboud University Medical Center (Netherlands), Sengkang General Hospital ( Singapore), National Cancer Center (Singapore), Baylor College of Medicine (USA), IRCCS Istituto Tumouri “Giovanni Paolo II” (Italy), University of Amsterdam (Netherlands), University of Antwerp (Belgium), UCSF Helen Diller Family Institute Cancer Center (USA), European Institute of Oncology IRCCS (Italy), University of Milan (Italy), Synergie Lyon Cancer, Plateforme de Bio-informatique 'Gilles Thomas' (France), Università degli Studi di Milano (Italy)

This research was funded by: Luxembourg Cancer Foundation, European Research Council, University of Leuven.

Availability of raw data: Data from the ICGC cohort includes: ICGC Data Portalthe data from ELBC includes: gene expression omnibus Accession number GSE88770 provides access to data from MINDACT. EORTCindividual patient read count data can be accessed below. bio keythe raw sequence reads include European Genomic Phenomena Archive Research No. EGAS00001004809 and data accession number. EGAD00001006608

Featured image credit: Photo provided National Cancer Institute upon unsplash

This summary was edited by: Aubrey Zirkle

Source: sciworthy.com

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