KRAS: feeding pancreatic cancer proliferation.
KRAS: feeding pancreatic cancer proliferation.
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DOI：
10.1016/j.tibs.2013.12.004
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发表时间：
2014-02
影响因子：
13.8
通讯作者：
Der, Channing J.
中科院分区：
文献类型：
--
作者：
Bryant, Kirsten L.;Mancias, Joseph D.;Kimmelman, Alec C.;Der, Channing J.
致癌基因KRAS突变是胰腺导管腺癌(PDAC)进展和生长的标志性基因事件，PDAC是一种几乎普遍致命的疾病。尽管人们已经意识到近95%的PDAC存在突变激活的KRAS，但到目前为止，还没有针对这种突变蛋白的有效治疗方法进入临床。许多研究表明，致癌的KRAS通过协调多种代谢变化，包括刺激葡萄糖摄取、葡萄糖中间体的差异通道、重新编程的谷氨酰胺代谢、自噬增加和巨噬细胞吞噬，在控制肿瘤代谢中发挥核心作用。在这里，我们回顾了这些最新的发现，并阐述了它们如何应用于开发新的PDAC治疗方法。
Oncogenic KRAS mutation is the signature genetic event in the progression and growth of pancreatic ductal adenocarcinoma (PDAC), an almost universally fatal disease. Although it has been appreciated for some time that nearly 95% of PDAC harbor mutationally activated KRAS, to date no effective treatments that target this mutant protein have reached the clinic. A number of studies have shown that oncogenic KRAS plays a central role in controlling tumor metabolism by orchestrating multiple metabolic changes including stimulation of glucose uptake, differential channeling of glucose intermediates, reprogrammed glutamine metabolism, increased autophagy, and macropinocytosis. Here we review these recent findings and address how they may be applied to develop new PDAC treatments.
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通讯作者：
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