PARP inhibition in cancer therapy

This study examines the chemoresistance of triple-negative breast cancer cell lines to PARP/PI3K dual inhibition and identifies treatment schedules that enhance its efficacy.

The paper investigates how FANCJ helicase affects PARP1 activity during DNA replication in BRCA1 deficient cells, revealing its role in PARPi efficacy and resistance.

The paper identifies MPC1 as a key driver of PARP inhibitor resistance in NSCLC lung cancer through a metabolism-focused CRISPR screen.

This paper uses causal inference to evaluate resistance mechanisms of DDR inhibitors in cancer, identifying pathway-specific resistance drivers and potential combination therapies.

The paper maps the genetic interaction network of PARP inhibitor response by analyzing 147,153 pairwise interactions and reveals hierarchical pathway organization and context-specific buffering interactions.

This study uses a multiomics approach to identify biomarkers of olaparib resistance and develops a predictive model to distinguish between responding and nonresponding cell lines.

This study shows that ARH3 deficiency causes cardiac dysfunction and that rucaparib, a PARP inhibitor, improves cardiac contractility and reduces infarct size in ARH3-deficient mice.

This study evaluates the impact of HRD status on clinical outcomes in Chinese EOC patients undergoing first-line chemotherapy and PARPi maintenance therapy, showing improved PFS and OS in HRD-positive patients.

The paper demonstrates that mammalian DNA undergoes reversible N1-adenosine PARylation, identified through mass spectrometry and enzymatic analysis.

The paper identifies p97 ATPase as a key player in removing trapped PARP1 from chromatin, enhancing PARPi-induced cytotoxicity in homologous recombination-defective cells.

This study identifies KDM6B as a key regulator of PARthanatos by modulating MGMT expression and checkpoint response in cancer cells exposed to alkylating agents.

The paper identifies transcriptional HRD (tHRD) based on aberrant transcript usage as a more accurate predictor of PARP inhibitor and DNA damaging agent responses than genomic HRD tests.

The paper identifies ADP-ribosylation sites regulated by HPF1 and ARH3 using proteomics, revealing widespread mono-ADP-ribosylation and challenges existing assumptions about PARP1 target residues.

This study investigates the dynamics of the HD subdomain in PARP-1 using NMR and crystal structures to understand its role in activation and inhibition.

The paper introduces a PAR photoaffinity probe to identify PAR-binding proteins, revealing novel binders and demonstrating length-selective PAR binding.

This study identifies genetic regulators of PARP inhibitor response using CRISPR screens, revealing TIP60 as a key factor that reverses PARPi sensitivity in BRCA2-deficient cells.

This study shows that combining Olaparib and Enzalutamide synergistically suppresses HCC progression by targeting AR-mediated miR-146a-5p/BRCA1 signaling.

The paper develops a multi-gene signature predicting PARP inhibitor response across cancer types using machine learning and validates it in vitro and in clinical datasets.

This paper describes a method to detect functional protein domains by identifying suppressor mutations in yeast and mouse cells, revealing insights into protein function and drug resistance mechanisms.