MTA 联合 PRMT5 抑制剂治疗 CDKN2A/MTAP 缺失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.
发表日期：2023 Nov 01
作者：
Kathleen M Mulvaney
来源：
Cancer Discovery
摘要：
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；肿瘤经常编码删除附近的基因 MTAP，从而产生对 PRMT5 的依赖。在本期《Cancer Discovery》中，Engstrom 及其同事报道了一种 MTA 合作的 PRMT5 甲基转移酶抑制剂 MRTX1719，它可以选择性杀死 CDKN2A/MTAP 编码缺失的癌症，并在针对携带 CDKN2A/MTAP 编码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 17 页。 2412 (1).©2023 美国癌症研究协会。
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).©2023 American Association for Cancer Research.