Mustachio Lisa Maria, Chelariu-Raicu Anca, Szekvolgyi Lorant, Roszik Jason
Department of Epigenetics and Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Center for Cancer Epigenetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Cancers (Basel). 2021 Mar 10;13(6):1204. doi: 10.3390/cancers13061204.
The Kirsten rat sarcoma viral oncogene homolog () is mutated in approximately 25% of all human cancers and is known to be a major player promoting and maintaining tumorigenesis through the RAS/MAPK pathway. Over the years, a large number of studies have identified strategies at different regulatory levels to tackle this 'difficult-to-target' oncoprotein. Yet, the most ideal strategy to overcome and its downstream effects has yet to be uncovered. This review summarizes the role of activating mutations in multiple cancer types as well as the key findings for potential strategies inhibiting its oncogenic behavior. A comprehensive analysis of the different pathways and mechanisms associated with activity in tumors will ultimately pave the way for promising future work that will identify optimum therapeutic strategies.
Kirsten大鼠肉瘤病毒癌基因同源物（）在所有人类癌症中约有25%发生突变，已知它是通过RAS/MAPK途径促进和维持肿瘤发生的主要因素。多年来，大量研究已经确定了在不同调控水平上应对这种“难以靶向”的癌蛋白的策略。然而，克服及其下游效应的最理想策略尚未被发现。本综述总结了激活突变在多种癌症类型中的作用以及抑制其致癌行为的潜在策略的关键发现。对与肿瘤中活性相关的不同途径和机制进行全面分析，最终将为确定最佳治疗策略的未来有前景的工作铺平道路。
