Anthony J. Davis

This study combines Msh2 depletion and proofreading-deficient DNA polymerase ε expression to enhance mutagenesis, enabling identification of drug resistance mutations and cytotoxin mechanisms in SCLC cells.

This study shows that LIPT1 loss causes replication stress and PARP inhibitor sensitivity via PrimPol-mediated ssDNA gaps in cancer cells.

This study evaluates carbon ion therapy's effectiveness in pancreatic ductal adenocarcinoma, finding that immune stromal components reduce its efficacy in vivo compared to in vitro results.

This study shows that dual inhibition of ATR and DNA-PKcs radiosensitizes ATM-deficient prostate cancer cells, with Compound B effectively achieving this in vitro and in vivo.

This study identifies PDAC cell lines defective in homologous recombination or with high genomic instability as more responsive to carbon ion radiotherapy, suggesting potential for targeted therapy.

The paper shows that TOP2B and DNA-PK regulate hypoxia-inducible gene expression through DNA topology changes, with DNA-PK phosphorylating TOP2B to control its activity.

This study identifies BUB1 as a regulator of non-homologous end joining (NHEJ) in triple-negative breast cancer (TNBC), showing that its inhibition sensitizes TNBC cells to radiotherapy.

This study identifies ATM phosphorylation of DNA-PKcs at T4102 as critical for stabilizing NHEJ machinery and promoting DSB repair.