**Molecular Pathogenesis of Gastric Adenocarcinoma**

**Molecular Pathogenesis of Gastric Adenocarcinoma**

DOI: 10.5772/intechopen.69951

Wei Kang, Jinglin Zhang and Ka Fai To Additional information is available at the end of the chapter

Wei Kang, Jinglin Zhang and Ka Fai To

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69951

#### **Abstract**

The incidence and mortality of gastric cancer (GC) rank top five and top three, respectively, among cancers around the world. It is an intricate malignancy caused by the reciprocity of intrinsically genetic, environmental, and host-related elements. The silent property, advanced clinical characterization, and potential heterogeneity have made GC a thorny disease with a high death rate. The increasing knowledge of the abundant genetic abnormalities regarding GC will definitely elongate the patients' survival. Scientists have been working hard to discover the myths beneath gastric tumorigenesis: novel biomarkers have been established, and cell transduction cascades have been well described. The study grouping GC into four molecular subtypes by The Cancer Genome Atlas (TCGA) broadens our horizon of GC etiologies. Knowledge regarding to the sophisticated networks in tumor microenvironment also bring new insights into the mechanisms assist GC development. In the future, people will strive for translating more research achievements into clinical utility. Successful translational medicine will lead to new methods for early GC diagnosis and precise medical strategies for individuals.

**Keywords:** gastric adenocarcinoma, molecular classification, pathogenesis

## **1. Introduction**

Gastric cancer (GC) is the fifth most common malignancy worldwide and third leading cancer-related death. Because of poor diagnosis, 5-year survival rate of GC is rather low, ranging from 15 to 52% [1, 2]. The incident rates are higher in men than in women. GC contributes over 20% of morbidity and mortality to cancer all over the world annually, following lung and liver cancer, which account for 23 and 28%, respectively. In 2012, approximate 723,000 deaths and more than 950,000 new GC cases were reported worldwide. Despite the incidence of GC has been declining in the North American and most of the west European countries, GC remains a type of prevailing cancer with increasing risk in regions including

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Asia, Eastern Europe, and certain areas of Latin America [3]. Particularly, adenocarcinomas, which developed from the glands of the most superficial layer or the mucosa, take up 90% of GC. The rest types of GC include mucosa-associated lymphoid tissue (MALT) lymphomas, which originate from the muscles surrounding mucosa areas of the stomach [4].

The risk factors include environmental factors, such as *Helicobacter pylori* infection, cigarettes smoking and high-salt diet, and host genetic alterations. Although the incidence of GC has shown a dramatic decrease in recent years due to *H. pylori* eradication, the overall survival is still quite poor due to its silent nature, late clinical presentation, and genetic heterogeneity. Thus, comprehensive understanding of the detailed molecular mechanisms and accurate pathogenesis of GC will improve patient outcome. Recently, several kinds of molecular classification of GC have been provided to reveal the genomic landscape of GC and decipher the crucial molecular changes. Among them, The Cancer Genome Atlas (TCGA) classification is a milestone for the molecular characterization of GC. Clinical translation of these molecular findings will provide novel strategies for early GC detection and promote precision therapies for GC patients.
