The biological model of gastric carcinogenesis.
The biological model of gastric carcinogenesis.
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发表时间：
2004
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通讯作者：
P. Correa
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作者：
P. Correa
胃癌发生的生物学模型可以被描述为一系列连续的阶段。第一种是对幽门螺杆菌感染的慢性活动性炎症反应。胃粘膜相关淋巴组织和多形核中性粒细胞的浸润以及上皮细胞的损伤是这一时期的特征。第二阶段主要是上皮细胞周期的改变，特别是细胞凋亡和细胞增殖率的增加。这些变化可能是多灶性萎缩的原因，多灶性萎缩是与癌症风险增加相关的胃炎类型的特征。第三，模型的更高级阶段显示出核和结构异常，这可能代表癌变的经典分子模型中预期的进行性突变事件。强调了全面看待生物模型的重要性。
The biological model of gastric carcinogenesis can be described as a series of sequential phases. The first consists of a chronic active inflammatory response to Helicobacter pylori infection. Infiltration of the gastric mucosa by mucosa-associated lymphoid tissue and polymorphonuclear neutrophils, as well as damage to the epithelial cells, characterize this phase. The second phase is dominated by alterations of the epithelial cell cycle, especially increased rates of apoptosis and cell proliferation. These changes may be responsible for the multifocal atrophy that characterizes the type of gastritis associated with an increased risk of cancer. The third, more advanced phase of the model displays nuclear and architectural abnormalities, which may represent progressive mutational events as expected in classical molecular models of carcinogenesis. The importance of a comprehensive view of the biological model is stressed.