APOBEC3 upregulation drives gemcitabine resistance Editorial

  


Authors: Maciejowski, J.; Mohamed, T.
Title: APOBEC3 upregulation drives gemcitabine resistance
Abstract: Gemcitabine is a widely used chemotherapy drug that acts by targeting DNA replication. Understanding why many tumors are unresponsive to gemcitabine is a clinical challenge. A new study in Nature Cancer reports that upregulation of the cytidine deaminases APOBEC3C and APOBEC3D facilitates resistance to gemcitabine by protecting cells against DNA replication stress. © Springer Nature America, Inc 2024.
Keywords: protein expression; protein phosphorylation; unclassified drug; gene mutation; genetics; nonhuman; note; gemcitabine; metabolism; antimetabolites, antineoplastic; drug effect; drug resistance; drug resistance, neoplasm; cell line, tumor; gene expression regulation; gene expression regulation, neoplastic; cytidine deaminase; genomic instability; tumor cell line; innate immunity; upregulation; single stranded dna; up-regulation; cellular stress response; deoxycytidine; antineoplastic antimetabolite; mutagenesis; chromosome 22; pancreatic ductal carcinoma; translesion synthesis; humans; human; crispr-cas9 system; apolipoprotein b mrna editing enzyme catalytic polypeptide like; apobec3a protein; apobec3b protein; doxecitine; apobec deaminases; apobec3 protein; apobec3c protein; apobec3d protein; apobec3 proteins, human
Journal Title: Nature Cancer
Volume: 5
Issue: 6
ISSN: 2662-1347
Publisher: Nature Research  
Date Published: 2024-07-01
Start Page: 818
End Page: 820
Language: English
DOI: 10.1038/s43018-024-00755-8
PUBMED: 38778178
PROVIDER: scopus
DOI/URL:

https://www.scopus.com/inward/record.uri?eid=2-s2.0-85193830105&doi=10.1038%2fs43018-024-00755-8&partnerID=40&md5=b3a6e46aea047350c730e30bacb70f9e
Notes: Note -- Source: Scopus
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MSK Authors
  1. John Maciejowski
    32 Maciejowski
  2. Taha Mohamed
    1 Mohamed
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