TL;DR
Investigations discovered KLF4 as a regulatory hub of DNA damage response and apoptosis evasion in BRCA2-mutated EOC and support targeting KLF4-driven anti-apoptotic pathways as a rational strategy to overcome PARP inhibitor resistance.
Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPis) induce regressions and extend progression-free survival (PFS) in ovarian cancer, especially in tumors with BRCA1 or BRCA2 mutations that impair homologous recombination repair. While recent studies have clarified the key roles of BRCA1, BRCA2, and PARP1 in replicat...
Cisplatin remains as standard chemotherapy for patients with HNSCC, but rapid development of drug resistance has limited patient benefit. The p53 tumor suppressor plays a central role in the cellular response to DNA damage in cancer, triggering apoptosis to prevent propagation of damaged cells in tumor development. TP5...
Metastatic castration-resistant prostate cancer (mCRPC) remains a leading cause of cancer-related mortality in men. Although poly(ADP-ribose) polymerase (PARP) inhibitors are approved for mCRPC patients with homologous recombination repair (HRR) deficiencies, clinical trials combining olaparib with PD-1/PD-L1 inhibitor...
Only limited benefit of PD-1/PD-L1 blockade in augmenting PARPi activity is suggested and the need for alternative strategies to sustain PARPi-induced immunity is highlighted.
It is suggested that elevated STN1 levels can partially compensate for BRCA2 loss by stabilizing stalled replication forks and limiting ssDNA gap accumulation, which is a major determinant of PARPi sensitivity in BRCA2-deficient cells.
BUB1 was significantly upregulated in UCEC tumors compared with normal endometrium, associated with advanced disease stage and reduced overall survival, confirming its role as an unfavorable prognostic biomarker and therapeutic target in UCEC.
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