A new study published in Science Translational Medicine reveals a counterintuitive mechanism by which ovarian cancer cells weaponize genomic instability to evade both immune surveillance and drug therapy. Researchers discovered that DNA damage in cancer cells activates the STING pathway, which paradoxically transforms normal fibroblasts into POSTN+ myofibroblasts that actively suppress immune function.
This transformation occurs through the STING-WNT signaling axis, creating an immunosuppressive tumor microenvironment that facilitates treatment resistance, particularly to PARP inhibitors. The findings challenge the conventional understanding of STING as purely a tumor suppressor, demonstrating instead how cancer cells exploit this immune surveillance pathway for their own benefit.
These insights identify new therapeutic targets for overcoming resistance mechanisms and improving treatment outcomes in ovarian cancer patients.
Read the full article on GMJ Newsroom.
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