论文部分内容阅读
胃肠道间质瘤(G IST)大多有C-K it的功能获得性突变,PDGFRα与C-K it属于同一家族,在C-K it呈野生型的G IST中发现存在PDGFRα功能获得性突变。酪氨酸激酶抑制剂(STI571)通过选择性抑制原癌基因ab l,Ab l-Bcr,C-K it和PDGF受体发挥作用,是无法手术的G IST病人的一线药物,但存在耐药性问题。
Gastrointestinal stromal tumors (GSTs) mostly acquire functional mutations in C-Kit, PDGFRα and C-Kit belong to the same family, and gain-of-function mutations in PDGFRα are found in G-ST in wild-type G-K it. Tyrosine kinase inhibitors (STI571) are first-line drugs in patients with GST that are inoperable by selective inhibition of the protooncogenes ab1, Ab1-Bcr, CKit and PDGF receptors, but are resistant to the problem .