Breaking The Prostate Cancer Hold

   July 23, 2012   

NEW YORK, NY (Marketwire – Jul 23, 2012)

The ability to distinguish the prostate cancers that will spread beyond the prostate and understand how they thrive is the crux of finding a prostate cancer cure. Breaking news suggests the protein SPDEF may hold the secret to prostate cancer’s success in surviving outside of the prostate, and could lead to very specific prostate cancer testing and treatment.

Dr. David Samadi, top prostate cancer surgeon, explains the role of SPDEF in prostate cancer metastasis. “When I remove a cancerous prostate through robotic SMART surgery, the goal is to prevent prostate cancer cells from leaving the prostate to take root in other healthy tissues,” he says. “Now, the presence of or lack of SPDEF appears to define whether or not the cells will survive if they do venture out.”

Researchers at the University of Colorado Cancer Center found that SPDEF-negative prostate cancer cells typically succeed in building new cancer colonies as they move throughout the body. However, when prostate cancer cells are SPDEF-positive they fail to establish new homes in the body and ultimately die off.

More specifically, the researchers believe SPDEF regulates the production of MMP9 and MMP13, proteins that facilitate cancer growth by attacking healthy tissue and making way for the cancer cells to grab on to new sites. If the prostate cancer cells can’t take root, they can’t invade new areas and grow.

As research continues, SPDEF could serve prostate cancer specialist and patients in two groundbreaking ways:

1) SPDEF Prostate Cancer Diagnosis – SPDEF-negative prostate cancer cells could help flag the most dangerous prostate cancers, while SPDEF-positive cells may predict those that will remain stuck in the prostate or travel but die off without life-threatening spread

2) SPDEF Prostate Cancer Treatment – gene therapy or nanodelivery could be used to alter SPDEF-negative prostate cancer cells by injecting the SPDEF protein and rendering them harmless outside of the prostate

“It’s the spread of prostate cancer that wreaks havoc,” says Dr. Samadi, “That’s what makes active surveillance or less aggressive treatments risky. But our limited ability to isolate variations in prostate cancer and predict the disease’s progression is also a challenge. Until we can say with certainty which prostate cancers will become metastatic, the best course is removal.”

The MMP9 and MMP13 proteins are known villains in the metastasis of breast, colon, lung, and ovarian cancers, as well. “Additional research involving SPDEF and the MMP proteins has the potential to impact cancer metastasis for a large number of patients, not just men with prostate cancer,” Dr. Samadi stressed.

Dr. David Samadi developed the SMART (Samadi Modified Advanced Robotic Technique) robotic prostatectomy surgery and is Vice Chairman of the Department of Urology and Chief of Robotics and Minimally Invasive Surgery at Mount Sinai Medical Center in New York.

       Press Release      

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