Characterization Of ERG, AR And PTEN Gene Status In Circulating Tumor Cells From Patients With Castration-Resistant Prostate Cancer
UroToday.com - The TMPRSS2-ERG gene fusion occurs in 30-70% of androgen deprivation therapy (ADT) naç¯ve prostate cancers (CaP), but its relevance in castration-resistant prostate cancer (CRPC) is less well defined. The TMPRSS2-ERG gene fusion is androgen driven. In the April 1, 2009 issue of Cancer Research, a group led by Dr. Johann de Bono evaluated patients undergoing treatment with the CYP17 inhibitor abiraterone acetate, which ablates the synthesis of androgens and estrogens that drive the TMPRSS2-ERG gene fusions. They hypothesized that androgen-dependent overexpression of ERG persisted in CRPC and that TMPRSS2-ERG tumors represented a subgroup of CaP that remained sensitive to abiraterone acetate. They hypothesized that two mechanisms of resistance to abiraterone acetate were gain of AR and loss of PTEN that could result in constitutive phosphorylation of AR, leading to ligand-independent activation.
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