Abstract
A recent report suggests that, in an in vitro model of premalignant breast cells (vHMECs), silencing of INK4A gene is accompanied by over-expression of cyclo-oxygenase (COX)-2. This suggests that COX-2 over-expression may be an early event in breast cancer aetiology permitting clones within the normal epithelium to evade apoptosis, to increase their numbers and perhaps acquire further changes that promote the formation of hyperplasias, and eventually carcinomas. While COX-2 expression in normal breast epithelium in vivo has not been proven to be linked to an increased risk of breast cancer, its over-expression in the premalignant model in vitro does provide preliminary evidence that COX-2 inhibition may be a useful chemoprevention strategy.
Highlights
The aetiology of breast cancer is complex but involves selection of variant cells that develop a growth advantage over and above that of the surrounding normal epithelium
The growth advantage must be a combination of increased proliferation and decreased apoptosis to allow cell survival
Comparison of normal breast tissue around cancer with breast reduction derived epithelium [1] indicated that it is mainly decreased apoptosis rather than increased proliferation that is seen in the normal epithelium in malignant breasts
Summary
The aetiology of breast cancer is complex but involves selection of variant cells that develop a growth advantage over and above that of the surrounding normal epithelium. A recent report from Crawford and coworkers [2] compared genes expressed in normal and variant human mammary epithelial cells (HMECs).
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