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PIK3CA gene aberrancy and role in targeted therapy of solid malignancies.
Cancer Gene Therapy ( IF 6.4 ) Pub Date : 2020-01-28 , DOI: 10.1038/s41417-020-0164-0
Owen Willis 1 , Khalil Choucair 2 , Abdurahman Alloghbi 1 , Laura Stanbery 3 , Rex Mowat 4 , F Charles Brunicardi 5 , Lance Dworkin 1 , John Nemunaitis 3, 6
Affiliation  

Phosphoinositide kinases (PIKs) are a group of lipid kinases that are important upstream activators of various signaling pathways that drive oncogenesis. Hyperactivation of the PI3K/AKT/mTOR pathways-either via mutations or genomic amplification-confers key oncogenic activity, essential for the development and progression of several solid tumors. Alterations in the PIK3CA gene are associated with poor prognosis of solid malignancies. Contradictory reports exist in the literature regarding the prognostic value of PIK3CA in aggressive cancers, but most available data highlights an important role of PIK3CA mutation in mediating tumorigenesis via increased signaling of the PI3K/AKT/mTOR survival pathway. Several inhibitors of PI3K/AKT/mTOR pathways have been investigated as potential therapeutic options in solid malignancies. This article reviews the role of PIK3CA mutations and inhibitors of the PI3K/AKT/mTOR pathway in cancer and examines association with the clinico-pathological parameters and prognosis.

中文翻译:

PIK3CA基因异常及其在实体恶性肿瘤靶向治疗中的作用。

磷酸肌醇激酶 (PIK) 是一组脂质激酶,它们是驱动肿瘤发生的各种信号通路的重要上游激活剂。PI3K/AKT/mTOR 通路的过度激活——通过突变或基因组扩增——赋予关键的致癌活性,这对于几种实体瘤的发展和进展至关重要。PIK3CA 基因的改变与实体恶性肿瘤的不良预后相关。文献中存在关于 PIK3CA 在侵袭性癌症中的预后价值的相互矛盾的报道,但大多数可用数据强调 PIK3CA 突变通过增加 PI3K/AKT/mTOR 存活途径的信号传导在介导肿瘤发生中的重要作用。已经研究了几种 PI3K/AKT/mTOR 通路抑制剂作为实体恶性肿瘤的潜在治疗选择。
更新日期:2020-01-28
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