Modulation of gene expression in ovarian cancer by active and repressive histone marks.

DNA methylation and histone modifications often function concomitantly to drive an aberrant program of gene expression in most cancers. Consequently, they have also been identified as being associated with ovarian cancer. However, several basic issues remain unclear - are these marks established early during normal ovarian functioning, or at a preneoplastic stage, or through a gradual accumulation, or do they arise de novo during transformation? Such issues have been difficult to address in ovarian cancer wherein preneoplastic lesions and progression models have not yet been established and drug-refractive disease progression is rapid and aggressive. The review presents an overview of the known involvement of histone modifications in various cellular states that might contribute to our understanding of epithelial ovarian cancer.