Prostate Cancer: Epigenetic Changes Point Toward New Treatments

New findings published in the journal Nature Genetics provide insight into how prostate cancer originates.

The second most common cancer in American men only to skin cancer, about 220,800 new cases are expected in 2015 with 27,540 ending in death, according to the American Cancer Society.

In the study, researchers worked to reprogram the master regulator of genes in prostate cells that drive malignant growth, giving them key insight into how prostate tumors take shape in the very beginnings of life.

Researchers first spotted evidence of cellular programming when they compared normal and cancerous prostate cells from several patients. During prostate cancer formation, the epigenetic formation is fundamentally altered. Researchers used the term "epigenetic" as it controls how genes operate but now how they make permanent changes in their DNA code. 

"What we have observed is that there is a new epigenetic program occurring as you transition from normal to tumor cells," co-study author Matthew Freedman, MD, of the Dana Farber Institute, said in a news release. "Maybe there will be a way to prevent this pattern from emerging, or perhaps we will be able to switch it back to the program being executed in normal cells."

As the tumors are fueled by testosterone, patients typically receive drugs that block testosterone from activating the androgen receptor--a protein activated by male hormones that turns on or off sets of genes controlling prostate cell growth and other functions. When examining prostate cancer patients, researchers found that the receptor bound to different sets of sites than in normal cells as they examined the androgen receptor.

"We observed that the binding pattern in one man's tumor looked a lot more like the pattern in another man's tumor than it did like the pattern in his own normal cells," added co-study author Mark Pomerantz, MD, physician at the Genitourinary Cancer Treatment Center at Dana-Farber.

In other words, according to Pomerantz, the androgen receptor had been reprogrammed to either activate or deactivate genes in such a way that it spurred prostate cells to both grow and spread abnormally.

Researchers are hopeful that with future research, it might be possible to reverse epigenetic reprogramming with the help of certain drugs aimed at epigenetic targets that either treat or even prevent prostate cancer.

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