Several attempts to classify gastric cancer (GCA) have been made over the past decades. Most successful, and widely used, is the classification by Laurén, which distinguishes, by microscopical morphology alone, two main cancer pathogeneses, diffuse (DGCA) and intestinal (IGCA) subtypes, which appear clearly as dissimilar clinical and epidemiological entities. Here we review the main differences in epidemiology, histopathology, and molecular pathology of the two main subtypes of gastric carcinomas based on Laurén classification. In clinical practice, however, clinical staging, particularly in predicting the survival, still remains superior to all classifications of gastric cancer independent of cancer type. The existence of local precursor lesions or conditions of IGCA tumours, i.e. Helicobacter pylori gastritis, atrophic gastritis (AG), intestinal metaplasia (IM), adenoma, dysplasia, and intramucosal neoplasia, is firmly established. The links of DGCA with intestinal-type epithelium, AG or IM are poor, or do not exist. So far, H. pylori gastritis is the only universal precursor condition for DGCA. It implies that AG and achlorhydria are of minor significance and infrequent in the development of DGCA but are important steps in that of IGCA. Despite an increasing body of data, the overall view on molecular pathology of GCA remains fragmentary. No consistent differences in the molecular pathology of GCA subtypes to meet the Laurén classification have been established. With the exception of TP53, no gene mutation occurring regularly in both histological types of GCA has been reported. Chromosomal aberrations and loss of heterozygosity seem to be non-specific and do not follow any consistent route in the progression of GCA. Microsatellite instability is more commonly found in IGCA than in DGCA. The present epigenetic data suggest that most of the decrease (or loss) of gene expression may be explained by promoter hypermethylation which is more often found in IGCA. In DGCA specific genes such as CDH1 are more often hypermethylated. Compared with GCA, in premalignant condition lesions gene mutations and chromosomal aberrations are infrequent. Epigenetic dysregulation might also represent a major mechanism for altered gene expression in premalignant stages in gastric carcinogenesis.

译文

在过去的几十年中,已经进行了几次对胃癌 (GCA) 进行分类的尝试。最成功且广泛使用的是lauren的分类,该分类仅通过显微镜形态学区分了两种主要的癌症病因,弥漫性 (DGCA) 和肠道 (IGCA) 亚型,它们显然是不同的临床和流行病学实体。在这里,我们根据lauren分类回顾了两种主要亚型胃癌流行病学,组织病理学和分子病理学方面的主要差异。然而,在临床实践中,临床分期 (尤其是在预测生存率方面) 仍然优于所有胃癌分类,而与癌症类型无关。IGCA肿瘤的局部前体病变或疾病的存在,即幽门螺杆菌胃炎,萎缩性胃炎 (AG),肠上皮化生 (IM),腺瘤,异型增生和粘膜内瘤变。DGCA与肠型上皮,AG或IM的联系较差或不存在。到目前为止,幽门螺杆菌胃炎是DGCA唯一的普遍前体疾病。这意味着AG和achlorhydria在DGCA的发展中意义不大,并不常见,但在IGCA的发展中却是重要的步骤。尽管有越来越多的数据,但对GCA分子病理学的总体看法仍然是零碎的。尚未建立符合Laurén分类的GCA亚型分子病理学的一致差异。除TP53外,没有报道在两种组织学类型的GCA中都定期发生基因突变。染色体畸变和杂合性丧失似乎是非特异性的,并且在GCA的发展过程中没有遵循任何一致的途径。微卫星不稳定性在IGCA中比在DGCA中更常见。目前的表观遗传数据表明,基因表达的大部分减少 (或丧失) 可以通过启动子高甲基化来解释,启动子高甲基化在IGCA中更常见。在DGCA中,特定基因 (例如CDH1) 通常被高甲基化。与GCA相比,在恶变前病变中,基因突变和染色体畸变很少。表观遗传失调也可能代表胃癌发生前恶性阶段基因表达改变的主要机制。

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