因为KRAS基因变异的高情况率基本在启动的和保持良性肿瘤出现中的至关重要性性,靶向疗法 KRAS便成的良好的缓解方法。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大家族中常用见基因变异的成員, KRAS基因变异在多个恶劣肿癌中以不同于的引发率出现了,其起病率以胰腺癌极限,此外是结十二指肠癌、非小神经细胞肝癌和胆管癌。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突然变化谱在有差别的 癌症复发种类两者存在着不错差别的,98%的KRAS突然变化是在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变化发生的在好多享有不相同变化规律的癌症晚期中,但变化亚型也现实存在的好大差异性。病患对KRAS G12控剂型的影响不相同,隐晦表示现实存在的底层耐药肺结核肺结核性,故此可以持续时间研究耐药肺结核肺结核性,以确立诊疗检验中拇指示酌情客户群体和癌症类型、的动物logo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.