A randomized multicenter Phase II study of docosahexaenoic acid in patients with a history of breast cancer, premalignant lesions, or benign breast disease Academic Article uri icon

Overview

MeSH Major

  • Adipose Tissue, White
  • Carcinoma, Squamous Cell
  • Inflammation
  • Tongue Neoplasms

abstract

  • © 2018 American Association for Cancer Research. Obesity, a cause of subclinical inflammation, is a risk factor for the development of postmenopausal breast cancer and is associated with poorer cancer outcomes. Docosahexaenoic acid (DHA), an omega-3 fatty acid, possesses anti-inflammatory properties. We hypothesized that treatment with DHA would reduce the expression of proinflammatory genes and aromatase, the rate-limiting enzyme for estrogen biosynthesis, in benign breast tissue of overweight/obese women. A randomized, placebo-controlled, double-blind phase II study of DHA given for 12 weeks to overweight/obese women with a history of stage I-III breast cancer, DCIS/LCIS, Paget's disease, or proliferative benign breast disease was carried out. In this placebo controlled trial, the primary objective was to determine whether DHA (1,000 mg by mouth twice daily) reduced breast tissue levels of TNFα. Secondary objectives included evaluation of the effect of DHA on breast tissue levels of COX-2, IL1β, aromatase, white adipose tissue inflammation, and gene expression by RNA-seq. Red blood cell fatty acid levels were measured to assess compliance. From July 2013 to November 2015, 64 participants were randomized and treated on trial (32 women per arm). Increased levels of omega-3 fatty acids in red blood cells were detected following treatment withDHA(P < 0.001) but not placebo. Treatment with DHA did not alter levels of TNFα (P = 0.71), or other biomarkers including the transcriptome in breast samples. Treatment with DHA was overall welltolerated. Although compliance was confirmed, we did not observe changes in the levels of prespecified biomarkers in the breast after treatment withDHAwhencompared with placebo.

publication date

  • April 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1158/1940-6207.CAPR-17-0354

PubMed ID

  • 29453232

Additional Document Info

start page

  • 203

end page

  • 214

volume

  • 11

number

  • 4