随着KRAS基因变异的高形成率以及在加载和形成肺部肿瘤成长中的注重性,靶点 KRAS便变成 一项不错的疗法战略。Targeting KRAS is a desirable strategy because of the high prevalence of KRAS mutations and its importance in initiating and sustaining tumor growth.KRAS是RAS家族性的中常用见变异的成員, KRAS变异在好几种恶变癌症中以各不相同的进行率导致,其患病率以胰腺癌极限,其二是结十二指肠癌、非小细胞膜肺肿瘤和胆管癌。KRAS is the most commonly mutated member of the Ras family,KRAS mutations are seen in a variety of malignancies at different rates,its incidence is highest in pancreatic cancers,followed by coleractal cancer,NSCLC and colangiocarcinoma.KRAS变动谱在多种肠癌类之間的存在同质性对比,98%的KRAS变动应用于G12、G13或 Q61。The profile of KRAS mutations differ significantly among diverse cancer types.98% of KRAS mutations are found at G12,G13,or Q61.KRAS基因甲基化率的发生在诸多具有着的差异基因甲基化率频繁的癌症复发中,但基因甲基化率亚型也具有巨大的差异。朋友对KRAS G12抑止剂的发应的差异,试探具有发挥抗药效肺结核性,以须得持继探索世界抗药效肺结核性,以知道监床耐压试验手指示非常合适众人和肉瘤种类的生物体标志牌物。KRAS mutations occur in many cancers with different mutation frequencies, but there is also a large
variation in mutation subtypes. The response to KRAS G12c inhibitors in patients is different, implicating the existence of resistance. Exploration of resistance should be conducted to identify biomarkers that indicate the appropriate population and tumor type in the clinical trial.