Literature DB >> 25711864

Avalanching mutations in biallelic mismatch repair deficiency syndrome.

Joshua J Waterfall1, Paul S Meltzer1.   

Abstract

Tumors from pediatric patients generally contain relatively few somatic mutations. A new study reports a striking exception in individuals in whom biallelic germline deficiency for mismatch repair is compounded by somatic loss of function in DNA proofreading polymerases, resulting in 'ultra-hypermutated' malignant brain tumors.

Entities:  

Mesh:

Year:  2015        PMID: 25711864     DOI: 10.1038/ng.3227

Source DB:  PubMed          Journal:  Nat Genet        ISSN: 1061-4036            Impact factor:   38.330


  3 in total

1.  Identification of Exo1-Msh2 interaction motifs in DNA mismatch repair and new Msh2-binding partners.

Authors:  Eva M Goellner; Christopher D Putnam; William J Graham; Christine M Rahal; Bin-Zhong Li; Richard D Kolodner
Journal:  Nat Struct Mol Biol       Date:  2018-07-30       Impact factor: 15.369

Review 2.  POLD1: Central mediator of DNA replication and repair, and implication in cancer and other pathologies.

Authors:  Emmanuelle Nicolas; Erica A Golemis; Sanjeevani Arora
Journal:  Gene       Date:  2016-06-16       Impact factor: 3.688

3.  The properties of Msh2-Msh6 ATP binding mutants suggest a signal amplification mechanism in DNA mismatch repair.

Authors:  William J Graham; Christopher D Putnam; Richard D Kolodner
Journal:  J Biol Chem       Date:  2018-09-20       Impact factor: 5.157

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.