The Many Faces of Obesity and Its Influence on Breast Cancer Risk
- 1National Cancer Institute (NCI), United States
- 2Division of Cancer Prevention, National Cancer Institute (NCI), United States
Obesity is associated with increased risk of breast and other cancers. However, the complexity of the underlying mechanisms, together with the interplay of diet and physical activity - contributing to energy balance - and the role of adipose tissue, pose challenges to our understanding of the basis of this increased risk. Epidemiologic studies have documented a higher obesity prevalence in US African-American (AA) and Hispanic women compared to Caucasian women. Elucidation of the contribution of potential biological differences among racially distinct groups to their differences in breast cancer (BC) risk and mortality have been topics of considerable interest in recent years. The racial and ethnic variation in body fat distribution may account for at least part of the differences in breast cancer rates in these populations. Yet, while AA women exhibit higher rates of obesity compared to white women, this does not translate directly into higher rates of BC. In fact, overall, BC in AA women occurs with a lower incidence than BC in white women. Obesity is a known risk factor for postmenopausal breast cancer, and growing evidence suggests that central obesity may increase risk for triple negative breast cancer, which is more common in premenopausal women. The positive association of postmenopausal BC risk and specifically estrogen receptor (ER)-positive BC, is presumably due largely to accumulation of estrogen in the adipose tissue of the breast and other tissues. Of the two main types of adipose tissue - subcutaneous and visceral – visceral adipocytes are more active metabolically. Such adipose tissue harbors multiple molecular entities that promote carcinogenesis: endocrine molecules/hormones, immunologic factors, inflammatory cytokines, metabolic alterations, and other components of the microenvironment. Expression of these culpable entities is largely regulated by epigenetic mechanisms. The interrelationship between these entities and drivers of epigenetic alteration are critical to the regulation of pathways connecting obesity and cancer risk. Initiatives to counteract the carcinogenic effects of obesity have primarily involved modulation of energy balance by diet. However, targeting of specific molecular abnormalities characterizing adiposity offers an alternative approach to preventing cancer. Our goal in this review is to first discuss the major mechanisms contributing
Keywords: Weight Loss, Epigenetics (MeSH), breast cancer risk, endocrine function, Adiposity (MeSH)
Received: 09 May 2019;
Accepted: 29 Jul 2019.
Edited by:Martine M. Bellanger, École des Hautes Etudes en Santé Publique, France
Reviewed by:Wagner R. Montor, Faculty of Medical Sciences, Santa Casa of Sao Paulo, Brazil
Parisa Tehranifar, Columbia University, United States
Copyright: © 2019 Agurs-Collins, Ross and Dunn. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Sharon Ross, National Cancer Institute (NCI), Division of Cancer Prevention, Rockville, 20892, Maryland, United States, firstname.lastname@example.org