DOI: 10.1097/01.OTU.0000399048.43246.af
,
Issn Print: 1742-8009
Publication Date: 2011/06/01
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Excerpt
Obesity is a well-known risk factor for postmenopausal breast cancer, but the molecular mechanisms behind obesity and an increased risk have been obscure. That situation may now be changing, according to Dr Andrew Dannenberg, speaking during the Joint AACR/ASCO Presidential Forum at the annual meeting of the American Association for Cancer Research.
His team has found, he said, that obesity and excess weight leads to inflammatory lesions in the breast tissue of mice and humans. Macrophages are a major component of these lesions, producing pro-inflammatory cytokines and triggering aromatase activity in mouse models of obesity.
The mechanistic link between excess weight, inflammation, and aromatase reveals potential therapeutic and prevention targets for breast cancer, particularly for hormone-receptor positive tumours. The data may also help explain the link between obesity and triple-negative breast cancer.
‘There are many, many examples of chronic inflammatory states predisposing to cancer', said Dr Annenberg, professor of medicine and director of the Weill Cornell Cancer Center, in a telephone interview after the meeting. ‘We have the first evidence that inflammation occurs in the human breast and it correlates with being overweight or obese, which are known risk factors for the development of postmenopausal breast cancer and also known to be terribly important in terms of negative prognosis for anyone afflicted with breast cancer.
‘This discovery is likely to be important for our current understanding and for developing rational interventions to try to attenuate this process', he said. ‘I think it may have profound public health implications.
