A PUBLICATION OF THE PATRICK C. WALSH PROSTATE CANCER RESEARCH FUND

The C-MYC Gene: If Controlled Early, Could it Stop Cancer?

angelo demarzo orostate cancer research
Angelo De Marzo
 Angelo De Marzo, M.D., Ph.D., a pathologist studying prostate cancer, has spent the last several years trying to go back in time. Studying endless slides of prostate tissue, starting with cancer and working his way back, past PIN (prostatic intraepithelial neoplasia — “funny looking” cells that are precursors for cancer), he discovered PIA —proliferative inflammatory atrophy — a chaotic, volatile mix of cells that seem to be dying, but are actually undergoing rapid change.

These cells could be headed toward cancer, but then again, they may be redeemable, with the right environmental changes. De Marzo, the Beth W. and A. Ross Myers Scholar, believes that inflammation plays an important role in PIA, and may be the cellular “last straw” that kicks these cells over into precancer — PIN.

This seems to start at the earliest
recognizable stage of prostate
cancer development.

Recently, De Marzo and his team have been investigating how a gene called C-MYC (pronounced C-“mick”) fits into this timeline. He got interested in this gene after work by Brady scientists William Isaacs and Jun Luo — who, with technological help, examined more than 10,000 genes in normal and cancerous prostate tissue — implicated C-MYC as a suspicious character. “C-MYC is known to function in many cancers as an oncogene — a cancer-causing gene,” explains De Marzo, “but scientists didn’t know when — or how often — the C-MYC gene became activated during the process of prostate cancer development.”

Now they have a pretty good idea. De Marzo’s research group has discovered that the C-MYC protein is cranked up in prostate cancer. “And, not only is it expressed in more than 80 percent of prostate cancers — previous estimates were around 25 to 50 percent — but this seems to start at the earliest recognizable stage of prostate cancer development, in PIN.” De Marzo’s work may enable C-MYC to become a biomarker in prostate cancer. “We also hope that it will inspire biomedical researchers to press hard to develop and test new ‘smart’ drug inhibitors of the C-MYC pathway in prostate cancer.”

 

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