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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Molecular pathology of gastric carcinoma
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Molecular pathology of gastric carcinoma

机译：胃癌的分子病理学

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Gastric carcinoma (GC) is a biologically heterogeneous disease involving numerous genetic and epigenetic alterations. A very small proportion of GCs can be caused by a specific germ-line mutation of the E-cadherin gene (CDH1). Sporadic GC is developed through multistep processes that begin with Helicobacter pylori-induced atrophic gastritis. Epstein-Barr virus is another infectious cause of GC, and the above two infection-associated GCs are characterized by global CpG island methylation in the promoter region of cancer-related genes. Mutations of tumor protein p53 (TP53) and β-catenin (CTNNB1) genes occur early in the development of GC and contribute to gastric carcinogenesis. Furthermore, significant numbers of GCs show loss of Runx3 due to hemizygous deletion and hypermethylation of the promoter region. Aberrant Cdx2 expression has been shown in precancerous lesions as well as GC. However, it remains unclear whether Cdx2 plays an oncogenic role in gastric carcinogenesis. GC with microsatellite instability is also a well-defined subset exhibiting distinctive clinicopathologic features. Targeted therapy against GC with ERBB2 amplification recently improved the prognosis of patients with advanced GC. In addition, epigenetic changes in GC could be attractive targets for cancer treatment with modulators. A genome-wide search has been undertaken to identify novel methylation-silenced genes in GC, which will help us understand the overall molecular features of GC and further provide novel opportunities in the treatment of GC.
机译：胃癌（GC）是一种生物异质性疾病，涉及许多遗传和表观遗传学改变。 E-钙粘蛋白基因（CDH1）的特定种系突变可能导致GC的比例很小。零星GC是通过多步过程开发的，从幽门螺杆菌诱发的萎缩性胃炎开始。爱泼斯坦-巴尔病毒是GC的另一种感染原因，上述两个与感染相关的GCs的特征是癌症相关基因的启动子区域中的整体CpG岛甲基化。肿瘤蛋白p53（TP53）和β-catenin（CTNNB1）基因的突变在GC的早期发生，并有助于胃癌的发生。此外，大量的GC显示由于半合子缺失和启动子区域的高甲基化而导致Runx3的丢失。 Cdx2异常表达已在癌前病变和GC中显示。但是，尚不清楚Cdx2是否在胃癌发生中起致癌作用。具有微卫星不稳定性的GC也是定义明确的子集，表现出独特的临床病理特征。针对具有GC的ERBB2扩增的靶向治疗最近改善了晚期GC患者的预后。此外，GC的表观遗传学改变可能是用调节剂治疗癌症的诱人靶标。已经进行了全基因组搜索以鉴定GC中新的甲基化沉默基因，这将有助于我们了解GC的整体分子特征，并进一步为GC的治疗提供新的机会。

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