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Abstract

Abstract 

  1. Adenocarcinoma comprises the vast majority of malignant tumors arising from the stomach. Gastric carcinoma is a significant worldwide health burden, second only to lung tumors as a leading cause of cancer deaths. Significant geographic and temporal variances are observed in this cancer's incidence, predominantly of the intestinal type. Epidemiologic studies indicate a strong environmental component in the acquisition of this cancer. Developing countries that are noted to have a high prevalence of Helicobacter pylori infection early in life are distinctly prone to having high rates of gastric adenocarcinomas. Most gastric cancers are identified in advanced stages that present in the later decades of adult life, commonly resulting in a lethal outcome shortly thereafter.

  2. Gastric cancers exhibit heterogeneity in clinical, biologic, and genetic aspects. Multiple pathologic classifications of gastric adenocarcinomas exist, including those with morphologic and histologic criteria. The TNM staging system is generally used as the basis for prognostication in this cancer, with depth of infiltration being an important parameter. Most cases of stomach cancer are sporadic in nature, with rare reports of inherited gastric cancer predisposition traits that can involve germ-line E-cadherin alterations or in conjunction with the hereditary nonpolyposis colon cancer disease entity.

  3. Cytogenetic studies have been unsuccessful in identifying an obvious significant chromosomal aberration in gastric cancers. Loss of heterozygosity studies and comparative genomic hybridization analyses have identified several loci with significant allelic loss, thus indicating the possibility of harboring a tumor-suppressor gene important in gastric tumorigenesis. The exact target(s) of loss or gain in most of these chromosomal regions, including 4q, 5q, 9p, 17p, 18q, and 20q, remains to be clarified. Additionally, evidence of Epstein-Barr virus infection can be found in a minority of gastric cancer patients.

  4. Multiple somatic alterations have been described in gastric carcinomas at the molecular level. The significance of these changes in gastric tumorigenesis remains to be established in most instances. The p53 gene is consistently altered in a majority of gastric cancer cases. Microsatellite instability and associated alterations of the transforming growth factor βII receptor, IGFRII, BAX, E2F-4, MSH3, and MSH6 genes are found in a subset of gastric carcinomas. Cell adhesion abnormalities such as E-cadherin or associated molecule alterations may play an important role in diffuse-type gastric cancer development. A detailed, clear working model of gastric tumorigenesis has yet to be formulated. Thus improved diagnostic, prognostic, therapeutic, and preventive strategies are eagerly awaited for gastric carcinomas. Critical molecular alterations that are prevalent in these cancers, once fully characterized, ultimately may provide new avenues to combat this lethal disease.

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