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n-3 Polyunsaturated Fatty Acids and Mechanisms to Mitigate Inflammatory Paracrine Signaling in Obesity-Associated Breast Cancer

Journal

NUTRIENTS
Volume 6, Issue 11, Pages 4760-4793

Publisher

MDPI
DOI: 10.3390/nu6114760

Keywords

breast cancer; inflammation; obesity; adipokines; n-3 polyunsaturated fatty acids; leptin; adiponectin; aromatase; lipid rafts; eicosanoids

Funding

  1. Natural Sciences and Engineering Research Council of Canada (NSERC)
  2. Ontario Graduate Scholarship
  3. NSERC

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Globally, the prevalence of obesity is increasing which subsequently increases the risk of the development of obesity-related chronic diseases. Low-grade chronic inflammation and dysregulated adipose tissue inflammatory mediator/adipokine secretion are well-established in obesity, and these factors increase the risk of developing inflammation-associated cancer. Breast cancer is of particular interest given that increased inflammation within the subcutaneous mammary adipose tissue depot can alter the local tissue inflammatory microenvironment such that it resembles that of obese visceral adipose tissue. Therefore, in obese women with breast cancer, increased inflammatory mediators both locally and systemically can perpetuate inflammation-associated pro-carcinogenic signaling pathways, thereby increasing disease severity. Herein, we discuss some of these inflammation-associated pro-carcinogenic mechanisms of the combined obese breast cancer phenotype and offer evidence that dietary long chain n-3 polyunsaturated fatty acids (PUFA) may have utility in mitigating the severity of obesity-associated inflammation and breast cancer.

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