Journal
MICROCIRCULATION
Volume 23, Issue 3, Pages 191-206Publisher
WILEY
DOI: 10.1111/micc.12270
Keywords
obesity; immune environment; desmoplasia; metformin; hypoxia; cytokines; IL-6; IL-1; VEGFR-1
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Funding
- Foundation for Science and Technology (Portugal, POPH/FSE funding program)
- National Institutes of Health [CA080124, CA085140, CA096915, CA115767, CA126642, CA197743]
- US Department of Defense [W81XWH-10-1-0016]
- Lustgarten Foundation
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With the current epidemic of obesity, a large number of patients diagnosed with cancer are overweight or obese. Importantly, this excess body weight is associated with tumor progression and poor prognosis. The mechanisms for this worse outcome, however, remain poorly understood. We review here the epidemiological evidence for the association between obesity and cancer, and discuss potential mechanisms focusing on angiogenesis and inflammation. In particular, we will discuss how the dysfunctional angiogenesis and inflammation occurring in adipose tissue in obesity may promote tumor progression, resistance to chemotherapy, and targeted therapies such as anti-angiogenic and immune therapies. Better understanding of how obesity fuels tumor progression and therapy resistance is essential to improve the current standard of care and the clinical outcome of cancer patients. To this end, we will discuss how an anti-diabetic drug such as metformin can overcome these adverse effects of obesity on the progression and treatment resistance of tumors.
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