打破癌基因成瘾：使RTK/RAS突变型癌症摆脱SOS依赖
Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS.
作者信息
Sheffels Erin, Kortum Robert L
机构信息
Department of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, United States.
出版信息
J Med Chem. 2021 May 27;64(10):6566-6568. doi: 10.1021/acs.jmedchem.1c00698. Epub 2021 May 7.
In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.
在RTK/RAS突变的癌症中，治疗抗性是由多种RTK的反弹激活驱动的；对RTK信号传导的广泛抑制可能会延迟大多数患者的治疗抗性。一种新的SOS1抑制剂BI-3406可广泛抑制近端RTK信号传导，这将大大提高用于治疗RTK/RAS突变癌症的疗法的疗效。
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