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Scientists have gained a key insight into how prostate tumors get their start – not by rewriting the normal DNA code, but by reprogramming the master regulator of genes in prostate cells to drive malignant growth.
The findings are a step toward understanding how prostate cancer originates and could open new opportunities for prevention and treatment, according to Dana-Farber Cancer Institute researchers reporting in Nature Genetics.
The researchers, led by Matthew Freedman, MD, and Mark Pomerantz, MD, said they have identified the “first mechanistic insights into a key set of events” that prods normal prostate cells down the road to cancer. It’s been a longstanding question, because few gene mutations have been found in prostate tumors. “This led us to wonder, is there another process going on?” said Freedman, of the Dana-Farber Center for Cancer Genome Discovery and Center Functional Cancer Epigenetics.
The investigators spotted evidence of the cellular reprogramming when they compared normal and cancerous prostate cells from several patients. It is termed “epigenetic” because it controls how genes operate but doesn’t make permanent changes in their DNA code. The androgen receptor is a protein activated by male hormones that turns on or off sets of genes that control prostate cell growth and other functions. The study demonstrated that this epigenetic program is fundamentally altered during prostate cancer formation.
Because epigenetic reprogramming can potentially be reversed, the authors say it might be possible in the future to use drugs aimed at epigenetic targets to prevent or treat prostate cancer.
Posted on October 12, 2015
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