Department of Gastroenterology, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece.
J Surg Res. 2011 Apr;166(2):255-64. doi: 10.1016/j.jss.2010.02.012. Epub 2010 Mar 6.
Chronic inflammation of the gastric epithelium has been associated with the pathogenesis of gastric cancer, as it was postulated by Corea's model of gastric carcinogenesis. Helicobacter pylori (Hp) regulates this inflammatory process and promotes gastric carcinogenesis through induction of gene mutations and protein modulation. Recent data raise the cancer stem cell hypothesis, which implies a central role of multipotent cancer cells in oncogenesis of various solid tumors. This review provides a synopsis of gastric cancer initiation and promotion through Hp and stem cell signaling pathways. The expanding research field of Hp-related cancer stem cell biology may offer novel implications for future treatment of upper gastrointestinal cancer.
胃上皮的慢性炎症与胃癌的发病机制有关,正如 Corea 的胃癌发生模型所假设的那样。幽门螺杆菌(Hp)通过诱导基因突变和蛋白调节来调节这一炎症过程,并促进胃癌的发生。最近的数据提出了癌症干细胞假说,这意味着多能癌细胞在各种实体肿瘤的发生中起着核心作用。本文综述了 Hp 和干细胞信号通路在胃癌发生和促进中的作用。Hp 相关癌症干细胞生物学这一不断扩展的研究领域可能为上消化道癌症的未来治疗提供新的启示。