Tumor-associated neutrophil precursors impair homologous DNA repair and promote sensitivity to PARP inhibition



Summary

Tumor-associated neutrophil precursors (TANPs) disrupt homologous recombination (HR), a crucial DNA repair mechanism, in cancer cells. TANPs achieve this by secreting factors that interfere with the proper function of HR proteins, leading to genomic instability. Consequently, cancer cells become more reliant on alternative repair pathways, like base excision repair. This dependence makes them highly vulnerable to PARP inhibitors, drugs that block base excision repair. In essence, TANPs indirectly sensitize tumors to PARP inhibition by crippling their primary DNA repair system. This finding suggests a potential therapeutic strategy of combining TANP-targeted therapy with PARP inhibitors to enhance cancer treatment efficacy.

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