引发胃肠道致癌程序。
Inflaming gastrointestinal oncogenic programming.
作者信息
DeNardo David G, Johansson Magnus, Coussens Lisa M
机构信息
Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
出版信息
Cancer Cell. 2008 Jul 8;14(1):7-9. doi: 10.1016/j.ccr.2008.06.010.
The etiology of gastrointestinal tumors implicates a role for chronic inflammation in response to pathogenic microflora as a promoting force for full neoplastic progression. Recently, Oguma and coworkers (2008) demonstrated that TNFalpha, derived from recruited macrophages, potentiates Wnt/beta-catenin signaling and gastric carcinogenesis by activating Akt signaling and GSK3beta phosphorylation independent of the NF-kappaB pathway in initiated epithelial cells. These observations provide a missing link in the mechanism whereby chronic inflammation, in response to Helicobacter, regulates the "penetrance" of initiating oncogenic mutations in the gastrointestinal tract leading to gastrointestinal tumorigenesis.
胃肠道肿瘤的病因表明，针对致病微生物群的慢性炎症作为肿瘤完全进展的促进因素发挥了作用。最近，小暮及其同事（2008年）证明，来源于募集的巨噬细胞的肿瘤坏死因子α（TNFα），通过激活Akt信号传导和糖原合成酶激酶3β（GSK3β）磷酸化，增强Wnt/β-连环蛋白信号传导和胃癌发生，且不依赖于起始上皮细胞中的核因子κB（NF-κB）途径。这些观察结果为慢性炎症响应幽门螺杆菌调节胃肠道起始致癌突变的“外显率”从而导致胃肠道肿瘤发生的机制提供了缺失环节。
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