According to a clinical study, a new type of cancer drug originally aimed at women with rare, inherited forms of breast and ovarian cancer may also help men with prostate cancer.
The drug stopped tumor growth in a third of men with a typically deadly form of advanced prostate cancer. Practically all of the patients who responded had related mutations in their tumors, which indicates the drug was targeting a common cell process.
Researchers reported these findings this week at the annual meeting of the American Association for Cancer Research.
The drug blocks an enzyme called poly polymerase, which helps cells repair a certain type of DNA damage. Oncologists are for the most part testing polymerase inhibitors in ovarian and breast cancer patients born with mutations in BRCA1 and BRCA2, two of the most infamous cancer-related genes.
These mutations raise a woman’s risk for breast and ovarian cancer as well as a man’s risk of prostate cancer. These mutations disable proteins that repair DNA damage that can result in additional cancer-spurring mutations. However flaws in either gene also make tumor cells vulnerable to polymerase inhibitors because the drugs additionally impair tumor cells’ DNA repair machinery. This combination renders tumor cells unable to fix DNA damage and they die an idea known as synthetic lethality.
AstraZeneca’s olaparib received approval in the United States and Europe for ovarian cancer patients who had inherited a BRCA1 or BRCA2 mutation.
In order to test their hypothesis, researchers gave the drug to men with metastatic castration resistant prostate cancer. Metastatic castration resistant prostate cancer means that the tumors have stopped responding to drugs that block the hormones that drive prostate cancer growth. Of the 49 men who stayed in the trial, 33% responded to the drug. Researchers classified responding to the drug in 3 categories, a drop in levels of tumor cells in the patient’ blood, a decline in blood levels of the biomarker prostate-specific antigen, or imaging scans that found heir tumors shrank.
After sequencing the patients’ tumor DNA researchers found that their assertion was correct.
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