Bishoy M. F. Hanna

TL;DR: A small-molecule drug that acts as a potent and selective active-site inhibitor that stops OGG1 from recognizing its DNA substrate and hampers Ogg1 binding to and repair of 8-oxoG is developed, which is well tolerated by mice and presents a proof of concept that targeting oxidative DNA repair can alleviate inflammatory conditions in vivo.

TL;DR: The potential treatment strategies, and the progress that has been made in developing inhibitors to core BER-proteins and related factors are discussed, are discussed.

TL;DR: OGG1 depletion obstructs A3 T-cell lymphoblastic acute leukemia growth in vitro and in vivo, validating OGG1 as a potential anti-cancer target and showing that O GG1 inhibitors (OGG1i) target a wide range of cancer cells, with a favourable therapeutic index compared to non-transformed cells.

TL;DR: In this paper, the effects of inactivating BER in OS conditions, by using a specific inhibitor of OGG1 (TH5487), were investigated. And the results demonstrate that OGG 1 is required to protect telomeres from OS and present OGG-1 inhibitors as a tool to induce oxidative DNA damage at Telomeres, with the potential for developing new combination therapies for cancer treatment.

TL;DR: This study validates TH5487 as a potent O GG1 inhibitor that prevents the repair of 8-oxoG and alters OGG1–chromatin dynamics and OGG 1′s recruitment kinetics.