IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal.
Helicobacter. 2011 Sep;16 Suppl 1:38-44. doi: 10.1111/j.1523-5378.2011.00879.x.
Gastric cancer (GC) is a world health burden, ranging as the second cause of cancer death worldwide. Etiologically, GC arises not only from the combined effects of environmental factors and susceptible genetic variants but also from the accumulation of genetic and epigenetic alterations. In the last years, molecular oncobiology studies brought to light a number of genes that are implicated in gastric carcinogenesis. This review is intended to focus on the recently described basic aspects that play key roles in the process of gastric carcinogenesis. Genetic variants of the genes IL-10, IL-17, MUC1, MUC6, DNMT3B, SMAD4, and SERPINE1 have been reported to modify the risk of developing GC. Several genes have been newly associated with gastric carcinogenesis, both through oncogenic activation (GSK3β, CD133, DSC2, P-Cadherin, CDH17, CD168, CD44, metalloproteinases MMP7 and MMP11, and a subset of miRNAs) and through tumor suppressor gene inactivation mechanisms (TFF1, PDX1, BCL2L10, XRCC, psiTPTE-HERV, HAI-2, GRIK2, and RUNX3). It also addressed the role of the inflammatory mediator cyclooxygenase-2 (COX-2) in the process of gastric carcinogenesis and its importance as a potential molecular target for therapy.
胃癌（GC）是全球健康负担之一，是全球癌症死亡的第二大原因。从病因学上讲，GC 的发生不仅与环境因素和易感遗传变异的综合作用有关，还与遗传和表观遗传改变的积累有关。近年来，分子肿瘤生物学研究揭示了许多与胃癌发生相关的基因。本文旨在重点介绍最近描述的在胃癌发生过程中起关键作用的基本方面。IL-10、IL-17、MUC1、MUC6、DNMT3B、SMAD4 和 SERPINE1 等基因的遗传变异已被报道可改变 GC 的发病风险。一些基因也与胃癌的发生有关，包括致癌基因激活（GSK3β、CD133、DSC2、P-Cadherin、CDH17、CD168、CD44、金属蛋白酶 MMP7 和 MMP11 以及一部分 miRNA）和抑癌基因失活机制（TFF1、PDX1、BCL2L10、XRCC、psiTPTE-HERV、HAI-2、GRIK2 和 RUNX3）。本文还探讨了炎症介质环氧合酶-2（COX-2）在胃癌发生过程中的作用及其作为治疗潜在分子靶点的重要性。
