(December 21, 2018) This month, researchers in Boston published their findings on how PARP inhibitors (PARPi) cause a chain reaction of responses from the tumor and its environment. Study authors, including OCRA grantee Ursula Matulonis, MD, treated BRCA-1 deficient tumors with olaparib, a PARPi, and found that it began both a natural and medically induced antitumor process that was STING (Stimulator of Interferon Genes) dependent. Meaning, the PARPi jump trigger the STING pathway, which then allows the PARPi to be efficient. They also found that, when olaparib is combined with PD-1 blockade, the efficacy of the treatment is amplified even more.
Understanding how PARPi work at the molecular level is an important step in making therapeutic strategies more efficient and, hopefully, translating that into better patient outcomes.
