Epigenetics as a mechanism driving polygenic clinical drug resistance.

ABSTRACT: Aberrant methylation of CpG islands located at or near gene promoters is associated with inactivation of gene expression during tumour development. It is increasingly recognised that such epimutations may occur at a much higher frequency than gene mutation and therefore have a greater impact on selection of subpopulations of cells during tumour progression or acquisition of resistance to anticancer drugs. Although laboratory-based models of acquired resistance to anticancer agents tend to focus on specific genes or biochemical pathways, such 'one gene:one outcome' models may be an oversimplification of acquired resistance to treatment of cancer patients. Instead, clinical drug resistance may be due to changes in expression of a large number of genes that have a cumulative impact on chemose

SUBMITTER: Glasspool RM 

PROVIDER: S-EPMC2361257 | biostudies-literature | 2006 Apr

REPOSITORIES: biostudies-literature