Although the P value (0.057) did not reach statistical significance because of the small sample size, and no post-treatment biopsies were available because of the original trial design, this finding provides further support for our hypothesis that sustained FGFR3 expression contributes to development of PARPi resistance.
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FGFR3-induced Y158 PARP1 phosphorylation promotes PARP inhibitor resistance via BRG1/MRE11-mediated DNA repair in breast cancer models.
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