MTA 合作 PRMT5 抑制剂治疗 CDKN2A/MTAP 缺失型癌症的早期临床成功。
Early Clinical Success of MTA-Cooperative PRMT5 Inhibitors for the Treatment of CDKN2A/MTAP-Deleted Cancers.
机构信息
Fralin Biomedical Research Institute, Virginia Polytechnic Institute and State University, Roanoke, Virginia.
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Blacksburg, Virginia.
出版信息
Cancer Discov. 2023 Nov 1;13(11):2310-2312. doi: 10.1158/2159-8290.CD-23-0951.
CDKN2A encodes the tumor suppressors p16 and p14ARF and is the most common homozygously deleted gene in all human cancers; tumors frequently codelete the nearby gene MTAP, creating a dependency on PRMT5. In this issue of Cancer Discovery, Engstrom and colleagues report an MTA-cooperative PRMT5 methyltransferase inhibitor MRTX1719 that selectively kills CDKN2A/MTAP-codeleted cancers and demonstrates early efficacy in clinical trials for solid tumors harboring the CDKN2A/MTAP codeletion. See related article by Engstrom et al., p. 2412 (1).
CDKN2A 编码肿瘤抑制因子 p16 和 p14ARF，是所有人类癌症中最常见的纯合缺失基因；肿瘤通常会同时缺失附近的基因 MTAP，从而产生对 PRMT5 的依赖性。在本期《Cancer Discovery》中，Engstrom 及其同事报告了一种 MTA 合作的 PRMT5 甲基转移酶抑制剂 MRTX1719，它可以选择性地杀死 CDKN2A/MTAP 缺失的癌症，并在含有 CDKN2A/MTAP 缺失的实体瘤的临床试验中显示出早期疗效。请参阅 Engstrom 等人的相关文章，第 2412 页（1）。
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