Anticancer duo kills tumors while avert degenerate

A new therapeutic approach for killing tumor cells simultaneously blocks both the PARP and RAD52 DNA repair pathway has.
The aptness of cancer cells to convalesce from treatment with PARP inhibitors (PARPis) stipulate that more burly and rapid elimination of BRCA-deficient tumor cells is statutory to prevent the time-dependent emergence of PARPi-resistant or stroppy clones. However, these cancers sometimes have a unique vulnerability, as the cancer cells have grow reliance on PARP to repair their DNA and accredit them to continue dividing.
The cancer cell over time turn to backup repair mechanisms and adapt to alternative repair pathways, a survival mode that also underlies their ability to evade targeted drug therapies.
“Cancers cells have multiple ways of protecting themselves from death,” said senior author Dr. Tomasz Skorski, professor of microbiology and immunology at Temple University. “The tumor cells eventually escape PARP1 inhibition by activating another backup to the BRCA-mediated repair pathway.
Our previous work had suggested that RAD52-dependent pathways are a likely escape route, which led us to see whether simultaneous inhibition of both PARP1 and RAD52 could trigger more effective lethality.”
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