Expression Signature

he prostate gland can be the site of multiple neoplastic transformation events, many of which give rise only to latent prostate cancer that does not progress to clinically detectable disease. While evidence of major subtypes of prostate cancer is lacking at the histopathological level, recent genomic analyses have provided increasing evidence for molecularly defined subtypes (Tomlins et al., Neoplasia 10(2):177-188, 2008; Palanisamy et al., Nat Med 16(7):793-798, 2010; Taylor et al., Cancer Cell 18(1):11-22, 2010) but expression profiling analyses of tumor specimens have not strictly defined molecular signatures associated with distinct subtypes that specifically correlate with disease outcome (Singh et al., J Androl 23(5):652-660, 2002a; Singh et al., Cancer Cell 1: 203-209, 2002b; Lapointe et al., Proc Natl Acad Sci USA 101(3):811-886, 2004; Tomlins et al., Nat Genet 39(1):41-51, 2007a; Tomlins et al., Nature 448(7153), 595-599, 2007b). However, oncogenomic pathway analyses that integrate analyses of gene expression, copy number alterations, and exon resequencing may provide a unified approach for distinguishing prostate cancer subtypes and stratifying patient outcome (Taylor et al., Cancer Cell 18(1):11-22, 2010). Integrating "omics" analyses with epigenetics will probably allow the identi- fication of true different subtypes of prostate cancers characterized by divergent biological behavior and/or response to therapy.