Integration of high resolution comparative analyses of naïve BAR-T and BEC20w cells revealed striking genetic and epigenetic changes induced by chronic acid and bile exposure that may disrupt normal cellular functions and promote carcinogenesis.
Three genes--CDKN1A, DDB2 and ADRB2--exhibited a trend towards loss of expression in melanomas thereby raising the possibility of a linked role in tumorigenesis.
Our results do not support a major independent role of ADRB2 polymorphisms in lung AC risk, suggesting that functional variants of other genes involved in the NNK epigenetic pathway of carcinogenesis should be investigated.