A landmark study published in Science Translational Medicine has uncovered a paradoxical mechanism by which genomic instability—long considered a cancer vulnerability—actually enables ovarian cancer cells to evade both immune surveillance and therapeutic intervention. Researchers discovered that DNA damage activates the STING pathway, which normally triggers immune responses against tumors. However, in the cancer microenvironment, this activation promotes the transformation of normal fibroblasts into POSTN+ myofibroblasts that actively suppress immune function. The transformed myofibroblasts operate through the STING-WNT signaling axis, creating a protective shield around cancer cells and promoting resistance to PARP inhibitor therapy. These findings fundamentally challenge our understanding of genomic instability as purely a therapeutic opportunity, revealing instead how cancer cells exploit damage-response mechanisms to their advantage. The research suggests that targeting the STING-WNT pathway in the tumor microenvironment may overcome current treatment resistance and improve clinical outcomes. Read the full article on GMJ Newsroom.
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