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Obesity and Cancer Risk: Controversy and Basic Biology

BCRF researchers share evidence-based lifestyle interventions to reduce cancer risk at the 2017 AACR Annual Meeting

The annual meeting of the American Association for Cancer Research (AACR) is historically focused on basic – or laboratory research. More recently, the meetings have incorporated sessions on ongoing clinical trials as a way to demonstrate how discoveries in the lab lead to real changes in patient care. In addition to clinical trial updates, the 2017 annual meeting from April 1-5 included several sessions on lifestyle and cancer risk and survivorship research, further linking basic science research to evidence-based interventions. In this edition of our AACR coverage we highlight talks on the obesity and cancer link featuring BCRF investigators, Andrew Dannenberg, Melinda Irwin, Dipali Sharma and Walter Willett.

Healthy Weight and Breat Cancer Risk

Lifestyle factors, most notably diet and exercise, have a clear link to cancer risk including breast cancer. We know that being overweight or obese (BMI of 25 or 30, respectively) increases the risk breast cancer after menopause and affects breast cancer outcomes at any age. There are many plausible theories that could explain the obesity-breast cancer link, but recent studies suggest that local inflammation is playing a key role in this association.

Recently, Dr. Andrew Dannenberg and BCRF colleagues Drs. Neil Iyengar and Clifford Hudis, reported the presence of an inflammatory marker called crown-like structures of the breast (CLS-B) in obese women with breast cancer. CLS-B are made up of a dead or dying fat cell surrounded by immune cells called macrophages that are essentially cleaning up the dead cell. This is a normal healing process that includes recruitment of other immune factors that create a localized inflammatory response, much like an injury would. In normal situations, the inflammatory response would clear up when the damage was repaired, but in the case of obesity, dying fat cells occur more frequently creating a chronic immune response and inflammatory environment that promotes breast cancer.

In his AACR presentation titled, “Breast Adipose Inflammation: A Silent Killer,” Dr. Dannenberg reported results from a follow up study including healthy weight women.  He explained that as much as 30 percent of the healthy weight women in the study had evidence of CLS-B that could potentially increase their risk of breast cancer in the absence of any obvious risk factors. A blood-based test to detect signs of inflammation could potentially identify women at increased risk of breast cancer and Dr. Dannenberg’s team is actively pursuing this strategy as well as looking for other non-invasive inflammatory biomarkers of risk.

In her presentation titled: “Inflammation and Cancer: the Role of Exercise,” Dr. Melinda Irwin presented data on a randomized control study of exercise that demonstrated a healthful benefit in reducing inflammation in the adipose tissue, supporting a role for physical activity to decrease risk, both locally by reducing inflammation and in maintaining a healthy weight.  In the same session BCRF investigator, Dr. Dipali Sharma demonstrated how a bioactive chemical called honokiol found in magnolia trees can convert white adipose, a source of inflammatory cytokines, to brown adipose and reduce leptin levels, a marker of inflammation.

Is Cancer Caused By Bad Luck?

Suggestions that most of cancer is due to bad luck stemming from accumulation of DNA damage that occurs during a lifetime of cell division were refuted in a widely attended forum at overflow capacity. The findings first reported in 2015 by investigators at Johns Hopkins recently garnered much media attention when a follow up study was released earlier this year. The study investigators contend that since the number of DNA mutations that occur during normal stem cell division is unpredictable and uncontrollable, cancer is due to bad luck.  While there is no argument from the scientific community that cancer is caused by DNA mutations, many argue that a statistical analysis of cell divisions over time, oversimplifies cancer risk and diminishes the impact of lifestyle, environmental and hereditary factors.

Presenting an argument for the latter, BCRF investigator, Dr. Walter Willett, one of the most referenced nutrition epidemiologists in the world, outlined work by his group and others that has shown how diet, diet composition, exercise, alcohol and tobacco use and other lifestyle choices impact DNA damage and contribute to the lifetime risk of cancer. The predictive impact of these lifetime exposures cannot be easily measured in mathematical models, but prevention strategies that promote healthy weight and lifestyle choices have been shown to reduce the risk of cancer. It was unfortunate, he said, that the press coverage of the study created the false illusion that if cancer is due to bad luck, individual behaviors have little impact on modifying that risk when the research clearly indicates otherwise.

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