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,已经进行了多次尝试来对胃癌(GCA)进行分类。最成功且应用最广泛的是Laurén的分类法,该分类法仅通过显微镜形态就可以区分出两种主要的癌症病原体,即弥散(DGCA)和肠道(IGCA)亚型,它们明显表现为不同的临床和流行病学实体。在这里,我们基于Laurén分类,回顾了两种主要胃癌亚型的流行病学,组织病理学和分子病理学的主要差异。然而,在临床实践中,临床分期,尤其是在预测存活率方面,仍然优于胃癌的所有分类,而与癌症类型无关。牢固地确定了局部局部前体病变或IGCA肿瘤的状况,即幽门螺杆菌胃炎,萎缩性胃炎(AG),肠化生(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的唯一通用先兆病状。这表明AG和胃酸缺乏症在DGCA的发展中意义不大,很少出现,但在IGCA中是重要的步骤。尽管有越来越多的数据,但关于GCA分子病理学的整体观点仍是零碎的。尚未建立符合劳伦分类的GCA亚型分子病理学方面的一致差异。除TP53外,在两种组织学类型的GCA中均没有定期发生基因突变的报道。染色体畸变和杂合性丧失似乎是非特异性的,并且在GCA的发展过程中未遵循任何一致的途径。在IGCA中比在DGCA中更常见微卫星不稳定性。目前的表观遗传学数据表明,基因表达的大多数减少(或丧失)可以通过在IGCA中更常见的启动子高甲基化来解释。在DGCA中,诸如CDH1之类的特定基因更经常被甲基化。与GCA相比,在癌变前病灶中,基因突变和染色体畸变很少见。表观遗传失调也可能代表了胃癌发生前癌变阶段基因表达改变的主要机制。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录