Abstract

Gastric cancer is a world health problem and depicts the fourth leading mortality cause from malignancy in Mexico. Causation of gastric cancer is not only due to the combined effects of environmental factors and genetic variants. Recent molecular studies have transgressed a number of genes involved in gastric carcinogenesis. The aim of this review is to understand the recent basics of gene expression in the development of the process of gastric carcinogenesis. Genetic variants, polymorphisms, desoxyribonucleic acid methylation, and genes involved in mediating inflammation have been associated with the development of gastric carcinogenesis. Recently, these genes (interleukin 10, Il-17, mucin 1, β-catenin, CDX1, SMAD4, SERPINE1, hypoxia-inducible factor 1 subunit alpha, GSK3β, CDH17, matrix metalloproteinase 7, RUNX3, RASSF1A, TFF1, HAI-2, and COX-2) have been studied in association with oncogenic activation or inactivation of tumor suppressor genes. All these mechanisms have been investigated to elucidate the process of gastric carcinogenesis, as well as their potential use as biomarkers and/or molecular targets to treatment of disease.

Highlights

  • Frontiers in MedicineRecent molecular studies have transgressed a number of genes involved in gastric carcinogenesis

  • Gastric cancer is a health problem, because it is the sixth leading cause of death worldwide [1]

  • This review focuses on recent aspects of gene expression in the development of gastric carcinogenesis

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Summary

Frontiers in Medicine

Recent molecular studies have transgressed a number of genes involved in gastric carcinogenesis. Gastric Cancer and Genetic Alterations with the development of gastric carcinogenesis These genes (interleukin 10, Il-17, mucin 1, β-catenin, CDX1, SMAD4, SERPINE1, hypoxia-inducible factor 1 subunit alpha, GSK3β, CDH17, matrix metalloproteinase 7, RUNX3, RASSF1A, TFF1, HAI-2, and COX-2) have been studied in association with oncogenic activation or inactivation of tumor suppressor genes. All these mechanisms have been investigated to elucidate the process of gastric carcinogenesis, as well as their potential use as biomarkers and/ or molecular targets to treatment of disease

INTRODUCTION
HOST GENETIC SUSCEPTIBILITY
MOLECULAR ALTERATIONS IN GASTRIC CANCER
GENETIC ABNORMALITIES
EPIGENETIC CHANGES PROMOTE THE DEVELOPMENT OF GASTRIC CANCER
WNT pathway
CONCLUSION
Findings
AUTHOR CONTRIBUTIONS

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