There are currently three different types of PARP inhibitors available to women with ovarian cancer. The drugs — which are all taken by mouth — are slightly different, but they all work more or less the same way in that they prevent cancer cells from naturally repairing the DNA that’s been damaged during the course of ovarian cancer treatment.
PARP inhibitors specifically work by blocking a protein that helps cancer cells repair their damaged DNA. “The easiest way to think of it is that, in general, cancer cells are broken,” says Dr. Willmott. “So they’re like someone who’s walking around with a broken leg and needs crutches to help them get around. In other words, they have certain cellular machinery that’s not working like it should. So they’re relying on less perfect forms of repair, like their PARP enzymes, to help them keep walking. PARP inhibitors are like taking away the crutches of someone with a broken leg. And unfortunately, then they can’t walk any longer. But for a cancer cell, that’s a good thing — because we want the cancer cell to die.”
PARP inhibitors are available to almost all women, though women with BRCA gene mutations or who are HRD proficient may benefit the most from these drugs. However, the American Society of Clinical Oncology (ASCO) released new guidelines recommending PARP inhibitors be offered to women, with or without genetic mutations, who are newly diagnosed with stage III or IV ovarian cancer and have improved with chemotherapy.
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Dr. Lyndsay Willmott is a gynecologic oncologist at Arizona Oncology. Read More
There are currently three different types of PARP inhibitors available to women with ovarian cancer. The drugs — which are all taken by mouth — are slightly different, but they all work more or less the same way in that they prevent cancer cells from naturally repairing the DNA that’s been damaged during the course of ovarian cancer treatment.
PARP inhibitors specifically work by blocking a protein that helps cancer cells repair their damaged DNA. “The easiest way to think of it is that, in general, cancer cells are broken,” says Dr. Willmott. “So they’re like someone who’s walking around with a broken leg and needs crutches to help them get around. In other words, they have certain cellular machinery that’s not working like it should. So they’re relying on less perfect forms of repair, like their PARP enzymes, to help them keep walking. PARP inhibitors are like taking away the crutches of someone with a broken leg. And unfortunately, then they can’t walk any longer. But for a cancer cell, that’s a good thing — because we want the cancer cell to die.”
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