Prostate cancer can often be successfully cured by removing the prostate gland and the cancerous tumor within it. But in men whose cancer has already begun to spread beyond the prostate, treating it successfully is much more difficult. Tumors in most patients develop resistance to the primary drug used to treat the disease, and long-term survival rates are low.
Now a researcher who studies how prostate tumor cells develop this resistance is hoping to find new ways of interfering with this cancer’s ability to evolve cells that are resistant to hormone therapy. Molecular biologist Ping Mu was recruited in 2018 to The University of Texas Southwestern Medical Center from Memorial Sloan-Kettering Cancer Center, where he was a postdoctoral researcher.
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Prostate cancer can often be successfully cured by removing the prostate gland and the cancerous tumor within it. But in men whose cancer has already begun to spread beyond the prostate, treating it successfully is much more difficult. Tumors in most patients develop resistance to the primary drug used to treat the disease, and long-term survival rates are low.
Now a researcher who studies how prostate tumor cells develop this resistance is hoping to find new ways of interfering with this cancer’s ability to evolve cells that are resistant to hormone therapy. Molecular biologist Ping Mu was recruited in 2018 to The University of Texas Southwestern Medical Center from Memorial Sloan-Kettering Cancer Center, where he was a postdoctoral researcher.
Cancer treatments exploit the fact that cancer cells “look” inherently different from normal cells. Targeted therapies, including chemotherapy, are designed to hone in on that difference in identity to kill the over-proliferating cancer cells.
Mu likens this targeting as being akin to having a photograph of a criminal in order to distinguish the culprit in a lineup of innocent people. “But cancer cells have the ability to switch their identity so they will look like someone else,” he says. “We call that ‘plasticity.’” Essentially that allows the criminal, i.e. cancer cell, to slip away and elude the hit squad. This means many therapies are often very effective in the beginning, but eventually most patients will develop resistance.
He is trying to find out how cancer cells can change identity, in an effort to try to shut down their ability to disguise themselves and escape. Mu is currently studying prostate cancer, but this phenomenon has also been reported in many different cancers, including breast and lung cancers. “So it might have a much wider impact if we can understand this identity shift,” he says.
Based on his research so far, Mu has already identified some key molecules that regulate plasticity, and has received a pilot grant from UT Southwestern to investigate new drug candidates that could target them.
Prostate cancer is the 2nd-most common cancer in American men, and more than 20,000 die from the disease each year. In addition to the problem of resistance, Mu is also looking at identifying the genetic differences between tumors that respond to hormone therapy and those that don’t. “We’re looking for new biomarkers to identify or predict patients’ responses so we can avoid giving them the wrong therapy,” he says.
The CPRIT award provides exceptional support, he says. “To fully understand how cancer cells develop resistance, you need not only money but also protected time to fully focus on research.”
He’s also found UT Southwestern to be exceptionally supportive of junior faculty. “The school creates environments for colleagues to come together from different areas of expertise,” he says, “and I learned very quickly in areas that I didn’t know before. Now I know who the experts are and who to go to, and I think that accelerates my research a lot.”
Mu received his undergraduate degree in biotechnology from Peking University in China, and his Ph.D. in cancer biology from Weill Cornell Medical College. He was a postdoctoral fellow at Sloan-Kettering starting in 2013.
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