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2016 ; 34
(35
): 4270-4276
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Obesity and Cancer Mechanisms: Tumor Microenvironment and Inflammation
#MMPMID27903155
Iyengar NM
; Gucalp A
; Dannenberg AJ
; Hudis CA
J Clin Oncol
2016[Dec]; 34
(35
): 4270-4276
PMID27903155
show ga
Purpose There is growing evidence that inflammation is a central and reversible
mechanism through which obesity promotes cancer risk and progression. Methods We
review recent findings regarding obesity-associated alterations in the
microenvironment and the local and systemic mechanisms through which these
changes support tumor growth. Results Locally, hyperadiposity is associated with
altered adipose tissue function, adipocyte death, and chronic low-grade
inflammation. Most individuals who are obese harbor inflamed adipose tissue,
which resembles chronically injured tissue, with immune cell infiltration and
remodeling. Within this distinctly altered local environment, several
pathophysiologic changes are found that may promote breast and other cancers.
Consistently, adipose tissue inflammation is associated with a worse prognosis in
patients with breast and tongue cancers. Systemically, the metabolic syndrome,
including dyslipidemia and insulin resistance, occurs in the setting of adipose
inflammation and operates in concert with local mechanisms to sustain the
inflamed microenvironment and promote tumor growth. Importantly, adipose
inflammation and its protumor consequences can be found in some individuals who
are not considered to be obese or overweight by body mass index. Conclusion The
tumor-promoting effects of obesity occur at the local level via adipose
inflammation and associated alterations in the microenvironment, as well as
systemically via circulating metabolic and inflammatory mediators associated with
adipose inflammation. Accurately characterizing the obese state and identifying
patients at increased risk for cancer development and progression will likely
require more precise assessments than body mass index alone. Biomarkers of
adipose tissue inflammation would help to identify high-risk populations.
Moreover, adipose inflammation is a reversible process and represents a novel
therapeutic target that warrants further study to break the obesity-cancer link.
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