DNA cytosine deamination is associated with recurrent Somatic Copy Number Alterations in stomach adenocarcinoma

Frontiers in Genetics

Genetics

Huangxuan Shen¹  Yilin Shi² 

[1] State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China;The College of Letters & Science, University of Wisconsin–Madison, Madison, WI, United States;

关键词: stomach adenocarcinoma;    DNA cytosine deamination;    hotspots;    Somatic Copy Number Alterations;    CCLE database;    TCGA database;   

DOI  :  10.3389/fgene.2023.1231415

 received in 2023-05-30, accepted in 2023-09-05,  发布年份 2023

来源: Frontiers

【 摘 要 】

Stomach Adenocarcinoma (STAD) is a leading cause of death worldwide. Somatic Copy Number Alterations (SCNAs), which result in Homologous recombination (HR) deficiency in double-strand break repair, are associated with the progression of STAD. However, the landscape of frequent breakpoints of SCNAs (hotspots) and their functional impacts remain poorly understood. In this study, we aimed to explore the frequency and impact of these hotspots in 332 STAD patients and 1,043 cancer cells using data from the Cancer Genome Atlas (TCGA) and Cancer Cell Line Encyclopedia (CCLE). We studied the rates of DSB (Double-Strand Breaks) loci in STAD patients by employing the Non-Homogeneous Poisson Distribution (λ), based on which we identified 145 DSB-hotspots with genes affected. We further verified DNA cytosine deamination as a critical process underlying the burden of DSB in STAD. Finally, we illustrated the clinical impact of the significant biological processes. Our findings highlighted the relationship between DNA cytosine deamination and SCNA in cancer was associated with recurrent Somatic Copy Number Alterations in STAD.

【 授权许可】

Unknown   
Copyright © 2023 Shi and Shen.