Liton Kumar Saha

TL;DR: It is shown that BRCA1 promotes MRE11-mediated removal of TOP2 adducts in G1 phase, which plays a critical role in removing pathological TOP2ccs induced by estrogens as well as etoposide throughout the cell cycle.

TL;DR: The purpose of this review is to summarize the current understanding of how the cell excises TOP-DPC and why, when and where the cell recruits one specific mechanism for repairing topoisomerase-mediated DNA damage, acquiring resistance to therapeutic topoisomersase inhibitors and avoiding genomic instability, cancers and neurodegenerative diseases.

TL;DR: In this article, a new ATR-based chemotherapy drug, M4344, was proposed and compared with the clinically developed ATR inhibitors BAY1895344, berzosertib, and ceralasertib using in vitro and in vivo models.

TL;DR: This review focuses on current knowledge of the protease pathways for debulking TOP-DPC and highlighting recent advances in understanding the mechanisms regulating the proteolytic repair pathways, including metalloprotease SPRTN/WSS1.

TL;DR: In this paper, the authors performed an unbiased genome-wide RNAi screen in SLFN11-WT and -knockout (KO) cells and found that inactivation of Ataxia Telangiectasia- and Rad3-related (ATR), CHK1, BRCA2, and RPA1 overcome chemoresistance to camptothecin (CPT) in cancer cells.