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Christopher E. Barbieri, MD, PhD, surgeon, researcher in prostate cancer genomics, Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine and New-York Presbyterian, discusses the implications of SPOP mutations in patients with prostate cancer.
Christopher E. Barbieri, MD, PhD, surgeon, researcher in prostate cancer genomics, Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine and New-York Presbyterian, discusses the implications of SPOP mutations in patients with prostate cancer.
The SPOP gene, which acts as a ubiquitin ligase, has mutations in approximately 10% to 15% of prostate cancers, which leads to an estimated 25,000 SPOP-mutant prostate cancers in 2016. SPOP-mutant prostate cancers look differently at the molecular level, Barbieri explains. This implies that this subtype will carry a different biology and, ultimately, will respond differently to standard therapies.
SPOP-mutant prostate cancers also have more genomic breaks and rearrangements. Research showed that SPOP mutations comprised the ability for prostate cells to repair their DNA. The clinical implications of this are important, he adds, because cells with repair challenges are susceptible to specific DNA-damaging therapy.
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