Vitamin A deficiency has been associated with the development of lung cancer in laboratory studies. However, clinical trials of natural and synthetic derivatives of vitamin A, called retinoids, for the prevention of lung cancer have been largely unsuccessful in the general population. A new study in the November 16 issue of the Journal of the National Cancer Institute finds that targeting a previously unknown variant of a common retinoid receptor may restore the beneficial effects of retinoids in lung cancer cells.
Retinoids help regulate certain cellular functions in the body, such as cell growth and differentiation. These effects are mediated by retinoic acid receptors (RARs), including RAR-beta. Clinical trials have supported a role for the use of retinoids in the prevention of aerodigestive tract cancers. However, large randomized trials of retinoids and retinoic acid have shown that they are ineffective--and may even be harmful--in preventing lung cancer in smokers. Laboratory studies have found that, as lung cancer develops, RAR-beta becomes silenced, which makes cells resistant to retinoids. This loss of expression of RAR-beta is often seen in the lung cells of smokers.
W. Jeffrey Petty, M.D., previously of Dartmouth Medical School and now a faculty member of the Wake Forest University School of Medicine in Winston-Salem, N.C., and colleagues at Dartmouth set out to discover the mechanisms responsible for RAR-beta silencing and to see if they could restore the expression of RAR-beta using a compound called azacytidine. In the process of studying human bronchial epithelial cells that were resistant to treatment with retinoic acid, they discovered a previously unknown variant of one of the subtypes of RAR-beta.
Kate Travis | EurekAlert!
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