Moss S F
Department of Medicine, St Luke's-Roosevelt Hospital Center/Columbia University, New York, NY 10025, USA.
Aliment Pharmacol Ther. 1998 Feb;12 Suppl 1:91-109. doi: 10.1111/j.1365-2036.1998.00002.x.
Gastric cancer is the end result of a chronic process, which usually starts as Helicobacter pylori-associated chronic gastritis. Although some differences exist in the histological intermediary stages and in the frequency and timing of certain molecular alterations, both diffuse and intestinal cancer are accompanied by some important common cellular changes. These include an increase in cell proliferation, and an alteration in apoptosis, which may be secondary to loss of function of p53 and loss of growth inhibition by growth factor (TGF)-beta, due to mutation of the TGF-beta receptor type II. This review examines the potential role of H. pylori in the aetiology of the molecular changes during the progression to gastric cancer, and explores the usefulness of these changes as biomarkers of increased risk of neoplasia in the intermediate steps of gastric carcinogenesis.
胃癌是一个慢性过程的最终结果，这个过程通常始于幽门螺杆菌相关的慢性胃炎。尽管在组织学中间阶段以及某些分子改变的频率和时间方面存在一些差异，但弥漫性癌和肠型癌都伴随着一些重要的共同细胞变化。这些变化包括细胞增殖增加和细胞凋亡改变，这可能继发于p53功能丧失以及生长因子（TGF）-β生长抑制作用丧失，后者是由于II型TGF-β受体突变所致。本综述探讨了幽门螺杆菌在胃癌进展过程中分子变化病因学中的潜在作用，并探讨了这些变化作为胃癌发生中间步骤中肿瘤形成风险增加的生物标志物的有用性。
