Journal
WORLD JOURNAL OF CLINICAL ONCOLOGY
Volume 8, Issue 2, Pages 106-119Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.5306/wjco.v8.i2.106
Keywords
Obesity-related cancer; Cancer stem cells; Leptin; Chemoresistance; Breast cancer; Pancreatic cancer
Categories
Funding
- Department of Defense (DOD), Congressionally Direct Medical Research Program (CDMRP) [W81XWH13-1-0382]
- National Institute of Health (NIH)/National Cancer Institute (NCI) [1R41CA183399-01A]
- MSM (Morehouse School of Medicine)/Tuskegee University/University of Alabama in Birmingham (UAB) Cancer Center [5U54CA118638]
- National Institute on Minority Health and Health Disparities (NIMHD) of NIH [5S21MD00101]
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Obesity is a major health problem and currently is endemic around the world. Obesity is a risk factor for several different types of cancer, significantly promoting cancer incidence, progression, poor prognosis and resistance to anti-cancer therapies. The study of this resistance is critical as development of chemoresistance is a serious drawback for the successful and effective drug-based treatments of cancer. There is increasing evidence that augmented adiposity can impact on chemotherapeutic treatment of cancer and the development of resistance to these treatments, particularly through one of its signature mediators, the adipokine leptin. Leptin is a pro-inflammatory, pro-angiogenic and pro-tumorigenic adipokine that has been implicated in many cancers promoting processes such as angiogenesis, metastasis, tumorigenesis and survival/resistance to apoptosis. Several possible mechanisms that could potentially be developed by cancer cells to elicit drug resistance have been suggested in the literature. Here, we summarize and discuss the current state of the literature on the role of obesity and leptin on chemoresistance, particularly as it relates to breast and pancreatic cancers. We focus on the role of leptin and its significance in possibly driving these proposed chemoresistance mechanisms, and examine its effects on cancer cell survival signals and expansion of the cancer stem cell sub-populations.
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