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DNMT3A Harboring Leukemia-Associated Mutations Directs Sensitivity to DNA Damage at Replication Forks.

Kartika VenugopalYang FengPawel NowialisHuanzhou XuDaniil E ShabashviliCassandra M BerntsenPrabhjot KaurKathryn I KrajcikChristina TaragjiniZachary ZaroogianHeidi L Casellas RománLuisa M PosadaChamara GunaratneJianping LiDaphné Dupéré-RicherRichard L BennettSanthi PondugulaAlberto RivaChristopher R CogleRene OpavskyBrian K LawSumita Bhaduri-McIntoshStefan KubicekPhilipp B StaberJonathan D LichtJonathan E BirdOlga A Guryanova
Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2021)
Together, our studies show that DNMT3A mutations underlie a defect in recovery from replication fork arrest with subsequent accumulation of unresolved DNA damage, which may have therapeutic tractability. These results demonstrate that, in addition to its role in epigenetic control, DNMT3A contributes to preserving genome integrity during replication stress.
Keyphrases
  • dna damage
  • dna methylation
  • genome wide
  • oxidative stress
  • dna repair
  • gene expression
  • acute myeloid leukemia
  • bone marrow
  • cell cycle
  • cell proliferation
  • soft tissue