Women who gain weight throughout adulthood have a greater breast cancer risk

March 01, 2016

This finding was observed among women who did not take hormone therapy after menopause.

Obesity is known to be a risk factor for developing breast cancer after menopause, according to background information in the article. Estrogens may accumulate in fat tissue, potentially initiating or promoting the growth of cancerous cells in the breast.

Jiyoung Ahn, Ph.D., of the National Cancer Institute, Bethesda, Md., and colleagues analyzed data from 99,039 postmenopausal women who were part of the National Institutes of Health??“AARP Diet and Health Study. In 1996, the women reported their current body measurements and weight, plus their weight at ages 18, 35 and 50. Body mass index (BMI) was used to classify the women as underweight, normal weight, overweight or obese.

Through 2000, 2,111 of the women developed breast cancer. In women who did not take menopausal hormone therapy, gaining weight in the early reproductive years (age 18 to 35), late reproductive years (age 35 to 50), perimenopausal and postmenopausal years (age 50 to the current age) and throughout adulthood (age 18 to the current age) were each associated with an increased risk of developing breast cancer compared with maintaining a stable weight during those periods.

Women who were not obese or overweight at age 18 but were at ages 35 and 50 had 1.4 times the risk of developing breast cancer compared with women who maintained a normal weight. Women who lost weight had the same breast cancer risk as those whose weight remained stable.

???Because weight gain during adulthood mainly reflects the deposition of fat mass rather than lean body mass, weight gain potentially represents age-related metabolic change that may be important in breast cancer development,??? the authors write. ???These findings may reinforce public health recommendations for the maintenance of a healthy weight throughout adulthood as a means of breast cancer prevention.???

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They also describe in their research work, that when the beta-F1-ATPase protein expression is inhibited or its activity reduced in the carcinomas, the tumour cells are forced to increase their intake of glucose by glycolytic means. Although this research trend is not new, since this same team already has reported in earlier work how the disruption of the mitochondrial bioenergetic function is a metabolic signature of tumours, and how this could be used in clinical prognosis of patients with colorectal, lung or breast cancer. Among other applications that the team and other research groups consider promising are the uses of this signature as a tool to predict the reaction of a patient to a treatment, or as a therapeutic target against cancer. The commercial applications of such prospective therapies are already protected by a patent that is owned by the ???Universidad Aut??noma de Madrid??? and is licensed to the Spanish biotechnology firm ???Fina Biotech, S.L???. Therefore this study might not sound like a new scientific discovery, but it provides the first evidence that integrates molecular and functional data supporting Warburg's hypothesis emphasizing the importance of the mitochondria in human pathology and more specifically in cancer biology.

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