Tag results:

PARP inhibitors

Poly(ADP-Ribose) Polymerase Inhibitors in Prostate Cancer: A Cornerstone in Precision Oncology

[Pharmacogenomics] Scientists summarize the key poly-(ADP-ribose) polymerase inhibitors, which act in cells with defects in homologous recombination DNA repair caused by genomic aberrations such as BRCA mutations, that are published and ongoing trials in prostate cancer.

Niraparib Exhibits a Synergistic Anti-Tumor Effect with PD-L1 Blockade by Inducing an Immune Response in Ovarian Cancer

[Journal of Translational Medicine] Programmed death ligand 1 (PD-L1) expression in human ovarian cancer cells after PARP inhibitors treatment was examined by western blotting and flow cytometry.

Germline Variants in DNA Repair Genes, including BRCA1/2, May Cause Familial Myeloproliferative Neoplasms

[Blood Advances] Investigators demonstrated the relevance of genetic germline diagnostics in elucidating the causes of myeloproliferative neoplasms (MPNs) and suggested novel therapeutic options in MPNs.

Synergistic Targeting of BRCA1 Mutated Breast Cancers with PARP and CDK2 Inhibition

[npj Breast Cancer] In cell lines, BRCA1 loss was associated with stabilized cyclin E1 during the cell cycle, and BRCA1 siRNA led to increased cyclin E1 in association with reduced phospho-cyclin E1 T62.

Understanding and Overcoming Resistance to PARP Inhibitors in Cancer Therapy

[Nature Reviews Clinical Oncology] Scientists summarize the diverse processes underlying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and discuss the potential strategies that might overcome these mechanisms such as combinations with chemotherapies, targeting the acquired vulnerabilities associated with resistance to PARP inhibitors or suppressing genomic instability.

Cell-Autonomous Inflammation of BRCA1-Deficient Ovarian Cancers Drives Both Tumor-Intrinsic Immunoreactivity and Immune Resistance via STING

[Cell Reports] Genetic deletion or methylation of DNA-sensing/IFN genes or CCL5 chemokine was identified as a potential mechanism to attenuate T cell inflammation.

Popular