What’s the Rationale for Adding PARP Inhibitors to Androgen Pathway Inhibitors for Patients with Prostate Cancer?
Over the last few years, the evidence has been mounting for the role of DNA repair in prostate cancer. What started with the Stand Up 2 Cancer (SU2C) International Dream Team discovery of 23% homologous recombination repair gene alteration rate in metastatic castration-resistant prostate cancer (mCRPC), followed by the identification of an 11.8% germline alteration rate in metastatic prostate cancer, has now led to broad sweeping successes with the introduction of PARP inhibitors to our clinics.1,2
The TRITON2 trial demonstrated a 43.5% objective response rate with rucaparib in patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious BRCA1 or BRCA2 alteration.3 This trial led to the United States Food and Drug Administration (FDA) granting accelerated approval to rucaparib for the
Evan Yu, MD
Evan Yu, a medical oncologist, treats prostate, bladder, and testicular cancer, and is passionate about providing a personalized medical approach to a selection of novel therapies as well as understanding biologic mechanism of drug sensitivity and resistance.
Medical Oncology, Translational Research, Novel molecular targeted agents, Biomarkers, Imaging (PET scans, MRI), Bone health.
- Professor, Department of Medicine, Division of Oncology, University of Washington School of Medicine
- Member, Clinical Research Division, Fred Hutchinson Cancer Research Center
- Clinical Research Director, Genitourinary Oncology, Seattle Cancer Care Alliance
- Medical Director, Clinical Research Service, Fred Hutchinson Cancer Research Consortium
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