Finding the Origin of Prostate Cancer to Stop Cancer Before it Starts

There was recently an exciting breakthrough in prostate cancer treatment. The ideal cancer treatment should be able to attack the source of uncontrolled cellular division at a minimal risk to the patient. In a new development, scientists have discovered a mechanism by which to eliminate prostate cancer by stopping the activity of just one enzyme known as PI5P4K?. The evidence of their clinical efforts was released in the journal Science Advances. While these discoveries have not reached human trials, their potential is undeniable.

Overcoming Treatment-Resistant Prostate Cancer

One of the biggest problems with traditional prostate cancer treatment (and most cancers in general) is that effective treatments become increasingly at risk of therapeutic resistance over time. Cancer cells are highly adaptive and can evolve ways to bypass cancer therapy over time. It can be thought of somewhat like an arms race.

Dr. Brook Emerling of the Sanford Burnham Prebys Medical Discovery Institute was the lead author of the study. Based on her experience, she believes that this research provides proof that highly targeted therapies can lead to excellent results. If stopping an enzyme works in prostate cancer, this will no doubt lead to advances in many cancer treatments, like pancreatic, skin, and breast cancer.

The main way that we treat Prostate Cancer today is through Androgen Inhibitors, drugs that suppress the production of Testosterone. This treatment works well, but up to 20% of men that go into remission will develop resistance to standard therapy by five years. If alternate methods of treatment aren't successful, the cancer can metastasize, and mortality risk skyrockets.

How Prostate Cancer Feeds off Testosterone

Prostate Cancer uses Testosterone and other Androgens to feed itself, causing the cancer to grow and to spread if left inadequately treated. Prostate Cancer uses the normal function of male sex hormones to promote its own development. Androgen Blockers work well because Prostate Cancer propagates most effectively in an androgen-rich environment.

Emerling explains that we need to learn exactly how Prostate Cancer originates and propagates so that we can create novel treatments that can significantly slow down the progression of prostate cancer and maybe even reverse its effects.

She is excited because targeted enzyme treatment gives hope to men that have developed resistance to Androgen Blockers or who have Prostate Cancer that thrives even when Testosterone is suppressed. With luck and ingenuity, we may eventually be able to treat Prostate Cancer without Androgen Suppression.

PI5P4K? Enzyme May Be Engine of Prostate Cancer Growth

Dr. Emerling and co-author Mark A. Rubin began investigating PI5P4K? because they observed that men with resistant, persistent prostate cancer showed elevated circulation of the enzyme. Based off of this information, the doctors hypothesized that PI5P4K? was the culprit that led to resistance and may even be critical to how all prostate cancers grow.

Emerling, Rubin, and their team analyzed the effects of PI5P4K? suppression through multiple advanced modeling systems for prostate cancer. These systems all demonstrated that by eliminating PI5P4K?, they could kill prostate cancer even for men that don't respond effectively to traditional treatment.

PI5P4K? is in a class of enzymes known as PI5P4Ks. These enzymes are important for lipid metabolism. Some vitamins are lipids, as are all fats and hormones. Researchers have just begun to understand the potential of treating cancer via targeted lipid metabolism inhibitors. If it's possible to target PI5P4K? specifically while maintaining the effectiveness of other PI5P4Ks, we can treat prostate cancer without affecting other critical avenues of fat metabolism.

Doctors Emerling and Rubin are in the process of creating drugs able to successfully suppress PI5P4K? and are not the only researchers seeking to do so. In a few years, these drugs are likely to enter clinical trial.

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