Mutation Found in Deadliest Prostate Cancer

May be key to therapy for often deadly, drug-resistant cancer

DNA Helix Illustration - One Different

A Cleveland Clinic researcher has discovered a genetic mutation in a drug-resistant, often deadly form of prostate cancer.

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The discovery may lead to new drug therapies to block the growth of the cancer.

Nima Sharifi, MD, the Kendrick Family Chair for Prostate Cancer Research at Cleveland Clinic, led the research which found the mutation that allows the tumor to make its own supply of androgens, a hormone that fuels the development castration-resistant prostate cancer (CRPC). Almost every man who dies of prostate cancer dies with this form of the disease.

“This gives us insight into the machinery tumors use to make androgens, and use that as a potential biomarker for resistance,” says Dr. Sharifi. “By finding this mutated enzyme we can now investigate treatments to block it.”

What is castration-resistant prostate cancer?

Prostate cancer requires a constant supply of androgens to sustain itself. The current standard treatment of metastatic prostate cancer patients is medical castration, which interferes with the body’s production of the androgen testosterone through drugs that disrupt the process.

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Castration-resistant prostate cancer is created when the metastatic prostate cancer thrives despite the lack of testosterone in the bloodstream. The tumors are able to exist without testosterone by creating androgens within the tumor cell — and the cancer keeps growing with usually fatal results.

Path to new drug therapy

In an era of personalized cancer care, the focus is on defining and treating cancer by its genetic abnormalities. Tumor-promoting enzyme mutations in several cancers have been identified and have led to development to targeted drug therapies, improving patient outcomes.

No targeted drug therapy against mutations currently exists for the standard treatment of metastatic CRPC.

But with this discovery that could change — and soon.

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“We have the opportunity for matching a mutant disease-driving biomarker with a pharmacologic inhibitor, drugs that can be added to clinical trials in the near future,” Dr. Sharifi says.

“Clinical utility could just be a few years away.”

 

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