TUESDAY, Nov. 15, 2005 (HealthDay News) -- New clues about the role of vitamin A resistance in lung cancer are detailed in a U.S. study.
The findings appear in the Nov. 16 issue of the Journal of the National Cancer Institute.
Laboratory studies have associated vitamin A deficiency with the development of lung cancer, according to background information in the study. However, human clinical trials of retinoids -- natural and synthetic derivatives of vitamin A -- for lung cancer prevention have been mostly unsuccessful.
This study, from researchers at Dartmouth, concluded that targeting a previously unknown variant of a common retinoid receptor called RAR-beta may help restore the beneficial effects of retinoids in lung cancer cells.
They found that this variant -- called RAR-beta-1' -- was expressed in normal lung cells and in cells sensitive to retinoic acid, but was not expressed in lung cancer cells or in cells resistant to retinoic acid treatment.
When the researchers treated cancer cells with a compound called azacytidine, RAR-beta-2 expression was restored but not RAR-beta-1' expression. This suggests that RAR-beta-1' has different characteristics and functions than other known forms of RAR-beta, and that it may play a role in retinoid resistance.
"Taken together, the data presented here directly implicate a critical role for RAR-beta-1' in mediating retinoid biologic effects in the lung and perhaps other organ sites," the study authors wrote.
"The frequent expression of RAR-beta-1' in lung carcinogenesis underscores its likely important biologic or clinical role," they wrote. "Identification of pharmacologic approaches that restore RAR-beta-1' expression would provide a basis for future retinoid-based combination strategies for lung cancer therapy or chemoprevention."
More information
The U.S. National Cancer Institute has more about lung cancer.
