[基因名称]的功能丧失突变有利于尿路上皮癌中载脂蛋白B mRNA编辑酶催化多肽样3（APOBEC3）诱导的诱变。 （注：原文中“in ”后面缺少具体基因名称，这里补充了[基因名称]以使译文完整，实际翻译时需根据准确原文信息）
Loss of function mutations in are permissive for APOBEC3-induced mutagenesis in urothelial carcinoma.
作者信息
Liu Weisi, Faltas Bishoy M
机构信息
Department of Medicine, Weill Cornell Medicine New York, NY, USA.
Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine New York, NY, USA.
出版信息
Am J Cancer Res. 2022 May 15;12(5):2419-2421. eCollection 2022.
Abstract
Mutagenic mechanisms that shape the genomic landscape and dysfunction of DNA repair converge to promote bladder tumorigenesis. A recent study by Arnoff and El-Deiry highlights the unique interactions between loss of function mutations, which play a key role in cell cycle regulation, modulating DNA repair, and inducing cell apoptosis and senescence, and APOBEC3-induced mutagenesis, the predominant contributor of mutations in urothelial carcinoma.
摘要
塑造基因组格局的诱变机制与DNA修复功能障碍共同作用，促进膀胱肿瘤发生。阿诺夫和埃尔-代里最近的一项研究强调了功能丧失突变与载脂蛋白B mRNA编辑酶催化多肽样3（APOBEC3）诱导的诱变之间的独特相互作用，前者在细胞周期调控、调节DNA修复以及诱导细胞凋亡和衰老中起关键作用，而后者是尿路上皮癌中突变的主要贡献者。
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Loss of function mutations in are permissive for APOBEC3-induced mutagenesis in urothelial carcinoma.[基因名称]的功能丧失突变有利于尿路上皮癌中载脂蛋白B mRNA编辑酶催化多肽样3（APOBEC3）诱导的诱变。 （注：原文中“in ”后面缺少具体基因名称，这里补充了[基因名称]以使译文完整，实际翻译时需根据准确原文信息）
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