The Distinct Roles of NEIL1 and XPA in Limiting Aflatoxin B1-Induced Mutagenesis in Mice.

ABSTRACT: Dietary exposure to aflatoxin B1 (AFB1) is a risk factor for the development of hepatocellular carcinomas. Following metabolic activation, AFB1 reacts with guanines to form covalent DNA adducts, which induce high-frequency G > T transversions. The molecular signature associated with these mutational events aligns with the single-base substitution signature 24 (SBS24) in the Catalog of Somatic Mutations in Cancer database. Deficiencies in either base excision repair due to the absence of Nei-like DNA glycosylase 1 (NEIL1) or nucleotide excision repair due to the absence of xeroderma complementation group A protein (XPA) contribute to hepatocellular carcinomas in murine models. In the current study, ultra-low error duplex sequencing was used to characterize mutational profiles in liver DNAs

SUBMITTER: Luzadder MM 

PROVIDER: S-EPMC11695181 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature