These effects are thought to result from changes in the expression of genes that regulate cell growth and differentiation. Like vitamin A deficiency, alterations in receptor expression or function could interfere with the retinoid signaling pathway and thereby enhance cancer development even in vitamin A sufficient individuals. The expression of the other receptors was not different among normal, dysplastic, and malignant oral tissues. However, the expression of RAR gamma and RXR beta was somewhat decreased in lung cancers. These results show that RAR beta expression is lost at early stages of carcinogenesis in the aerodigestive tract and support the hypothesis that the loss of RAR beta expression may facilitate the development of some of these cancers.
Gastrointestinal cancer remains a significant public health threat in developed countries.
The molecular biology of colon cancer has been well studied and it is an excellent model for the development of chemopreventive interventions. This fact allows clinical investigato- rs to utilize what is known about discrete biological phases of colon carcinogenesis to tailor clinical trial protocols that may attenuate a future risk for cancer. Among the agents currently in clinical trial testing are anti-oxidants, modulators of metabolism, and antiproliferatives. Current clinical trials have often incorporated the use of biomarkers as intermediate endpoints to assess the efficacy of particular preventives. The current status of ongoing colon cancer prevention trials suggests that this disease, in particular, may well be suited to chemopreventive approaches.