News Brief
Robbing Cancer Cells of Drug Resistance
January 29, 2025
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Approximately 5-10% of breast cancers and 10-15% of ovarian cancers involve BRCA-deficient tumors, caused by mutation or loss of BRCA1 or BRCA2 DNA-repair genes. Anti-cancer drugs called PARP inhibitors (e.g., Lynparza and Talzenna) can defeat these tumors by creating gaps in tumor-cell DNA that BRCA1/2-deficient tumor cells can’t repair. But unfortunately, resistance of BRCA-deficient tumors to PARP inhibitors has become a major problem.
In a recent study published online on January 16 in the Journal of Medicinal Chemistry, Vern L. Schramm, Ph.D., and colleagues report developing molecules that—when added to BRCA-deficient tumors that had become resistant to PARP inhibitors—restored the tumors’ sensitivity to the inhibitors. Known as transition-state analogs, these molecules target the enzyme DNPH1, which protects tumor cells from PARP inhibitors’ damaging effects. The transition-state analogs were synthesized by collaborators at the Ferrier Research Institute, Victoria University of Wellington, New Zealand.
Dr. Schramm is professor of biochemistry and the Ruth Merns Chair in Biochemistry at Einstein and a member of the National Cancer Institute-designated Montefiore Einstein Comprehensive Cancer Center.
Albert Einstein College of Medicine has filed patent application related to this research and is seeking licensing partners able to further develop and commercialize this technology. Interested parties can contact the Office of Biotechnology and Business Development at biotech@einsteinmed.edu.