CHICAGO – The protein known as phosphatase and tensin homolog (PTEN) is frequently mutated or affected by cancer as tumors develop. Now a new study from the Basser Center for BRCA at the Abramson Cancer Center of the University of Pennsylvania shows PTEN may serve as a marker for whether a patient with BRCA 1-2 deficient ovarian cancer is likely to respond to checkpoint inhibitor therapy. Researchers found the tumors that had PTEN loss were less likely to generate an immune response than tumors that maintain PTEN levels. They will present their findings at the American Association for Cancer Research Annual Meeting in Chicago on Wednesday (Presentation #5729).
BRCA1/2-deficient ovarian cancer is a specific subset of ovarian cancer. Genes known as BRCA1 and BRCA2 are involved in cell growth and the repair of damage to DNA. Mutations or deficiencies in these genes can cause DNA to go unrepaired, which increases the chance of developing cancer. These cancers are often initially susceptible to treatments that damage the tumor’s DNA, such as platinum chemotherapy, but most develop resistance and require other treatment strategies. One strategy is the use of anti-PD1/PDL1 immunotherapies. Although clinical trials have collectively shown a disease control rate
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