Study in JNCI also identified a molecular signature that distinguishes the TMPRSS2-ERG subtype from other malignancies.

Researchers pinpointed estrogen as a key player in about half of all prostate cancers. They found that estrogen-linked signaling helps drive a discrete and aggressive form of the disease caused by a chromosomal translocation, which in turn results in the fusion of two genes, TMPRSS2-ERG.

The team analyzed 455 prostate cancer samples that were placed in fixative and not frozen. The samples came from trials in Sweden and the U.S. that were conducted as far back as the mid-1970s.

To analyze the fixative samples, the team developed a technology for effectively reading the gene transcription profiles hidden in the samples. “That led us to perform the largest gene-expression microarray analysis yet conducted in prostate cancer research, amassing information on more than 6,000 genes,” states study senior author, Mark A. Rubin, M.D., professor of pathology and laboratory medicine and vice chair for experimental pathology at Weill Cornell Medical College.

“This allowed us to obtain a robust, 87-gene expression signature that distinguishes fusion-positive TMPRSS2-ERG cancers from other prostate malignancies.” A close analysis of the signature showed that estrogen-dependent molecular pathways appear to play a crucial role in regulating and encouraging this aggressive subset of prostate cancer.

“Our results suggest a mechanism by which prostate cancers might develop androgen independence from an initial androgen-dependent state,” the authors write in their research paper.

Dr. Rubin conducted the study while at the Brigham and Women’s Hospital in collaboration with members of the Broad Institute of MIT and Harvard. The findings are published in the May 27 online edition of the Journal of the National Cancer Institute.

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