Obesity May Remove a Natural Defense Against Breast Cancer
Sep 10, 2026
Read Time: 3 minutes
Takeaways:
Obesity may increase breast cancer risk partly by removing a natural defense. The researchers found that fat cells in lean breast tissue produce a lipid that helps suppress cancer, while fat cells in obese breast tissue produce less of it.
Lean fat cells produce more of a certain lipid, or fatty acid, which can trigger a form of cell death that kills damaged or cancerous cells.
With obesity, the fat cells in the breast change and stop secreting this lipid. This allows breast cancer cells to avoid cell death and grow more readily.
Impact: As this lipid is naturally produced in the body, researchers are interested in whether restoring or increasing it could become a future therapeutic strategy.
A research team at Huntsman Cancer Institute at the University of Utah (the U) has found that obesity prevents a biological process that kills cancerous cells, revealing a possible reason why obesity is a risk factor for breast cancer.
“We uncovered the role of a molecule that normally appears in lean tissue that restrains breast cancer growth but is less present with obesity,” says Keren Hilgendorf, PhD, Huntsman Cancer Institute investigator, assistant professor of biochemistry at the U, and senior author of the study. “We know obesity is often a driver of breast cancer, and researchers in our field usually consider how obesity is promoting the disease. But we hadn’t really considered that obesity could also be the loss of something that naturally protects us.”
Hilgendorf and first author Meghan Curtin, doctoral candidate in molecular biology at the U, have published the transformative results of their research in the prestigious journal Science.
"We hadn’t really considered that obesity could also be the loss of something that naturally protects us."
Keren Hilgendorf, PhD
Breasts are mostly composed of fat, particularly fat cells called adipocytes. These adipocytes are different depending on a person’s weight and can be lean or obese. In obesity, adipocytes are larger than in their lean counterparts. Hilgendorf also says that the two types of adipocytes generate distinctive microenvironments for cancer cells.
In preclinical models, including breast tissues from donors, Hilgendorf and Curtin found that one of those key differences is the production of a lipid, or fatty acid, known as 9S-HODE.
9S-HODE plays an important role in promoting cell death, particularly a kind of cell death called ferroptosis. This is one way the body purges old and damaged cells, including cells that could be cancerous.
“We found that the lean adipocytes produce much more 9S-HODE than obese ones. This means that cancerous cells die more readily in lean tissue,” says Curtin. “By producing more 9S-HODE, our bodies are actively protecting us, under lean circumstances, in a way it cannot with obesity.”
"We believe this shift in the understanding of the roles of lean and obese adipocytes is the start of something. This is just one discovery."
Meghan Curtin, Doctoral Candidate
In their preclinical mouse models, Hilgendorf and Curtin found that increasing the amount of 9S-HODE in obese adipocytes suppressed breast cancer tumor growth. They believe this new understanding could lead to better therapies.
“From a clinical perspective, this discovery is incredibly empowering. Because 9S-HODE is naturally present in the body but is lost with obesity, we may be able to restore this protection by putting it back,” says Hilgendorf. “That could become a very feasible therapeutic approach to slow breast cancer growth.”
Hilgendorf and Curtin recognize that obesity is just one factor that contributes to breast cancer and that the disease can develop for other reasons. They also say that 9S-HODE seems to be primarily produced by fat cells in the breast, though other fat cells throughout the body may have a similar protective function that will require more research.
“We believe this shift in the understanding of the roles of lean and obese adipocytes is the start of something. This is just one discovery, and it’s not the end of the road,” says Curtin. “This opened our eyes to new ways to think about science, and hopefully we can harness what our bodies are already doing to make progress against this disease.”
The critical research happening every day at Huntsman Cancer Institute is supported by the National Institutes of Health/National Cancer Institute, including cancer center support grant P30 CA042014, as well as Huntsman Cancer Foundation.
Media Contact
Heather Simonsen
Associate Director, Public Affairs
Huntsman Cancer Institute
801 646-4120
public.affairs@hci.utah.edu
About Huntsman Cancer Institute at the University of Utah Huntsman Cancer Institute at the University of Utah is the National Cancer Institute-designated Comprehensive Cancer Center for Utah, Idaho, Montana, Nevada, and Wyoming. With a legacy of innovative cancer research, groundbreaking discoveries, and world-class patient care, we are transforming the way cancer is understood, prevented, diagnosed, treated, and survived. Huntsman Cancer Institute focuses on delivering the most advanced cancer healing and prevention through scientific breakthroughs and cutting-edge technology to create pioneering cancer treatments beyond the standard of care today. We have more than 400 open clinical trials and more than 300 research teams studying cancer. More genes for inherited cancers have been discovered at Huntsman Cancer Institute than at any other cancer center. Our scientists are world-renowned for understanding how cancer begins and using that knowledge to develop innovative approaches to treat each patient’s unique disease. Huntsman Cancer Institute was founded by Jon M. and Karen Huntsman.
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