TMPRSS2-ERG fusion prostate cancer is a molecularly distinct estrogen-sensitive subclass of aggressive prostate cancer

ABSTRACT: Common epithelial cancers are believed to become more aggressive through the accumulation of multiple independent molecular events that lead to the deregulation of cell signaling. However, the discovery that the majority of prostate cancers harbor gene fusions of the 5'-untranslated region of androgen regulated TMPRSS2 promoter with ETS transcription factor family members has brought this paradigm into question1,2. TMPRSS2-ERG gene fusion is the most common molecular sub-type of prostate cancer. Recent work suggests that the TMPRSS2-ERG fusion is associated with a more aggressive clinical phenotype3. In the most advanced castration resistant prostate cancers where the androgen receptor has been inactivated, the TMPRSS2-ERG fusion remains functionally active. Here we show compelling clinica

ORGANISM(S): Homo sapiens

SUBMITTER: Mark Rubin 

PROVIDER: E-GEOD-8402 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress