Gastric cancer carcinogenesis and tumor progression

Giovanni Corso, Raquel Seruca, Franco Roviello

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: Gastric cancer (GC) remains one of the leading causes of cancer-related deaths worldwide, even though a decline has been observed in its incidence and the mortality rate in recent decades. Gastric carcinogenesis is a complex phenomena involving multiple epigenetic and genetic factors; several genetic, environmental and infectious agents interact causing a cumulative effect in the early steps of gastric carcinogenesis. Materials and Methods: The most commonly used classifications of GC are the World Health Organization (WHO) and the Laurén classifications which describes two main histological types, diffuse and intestinal, which have different clinicopathological characteristics. Diffuse cancer occurs more commonly in young patients, can be multifocal, is not often accompanied by intestinal metaplasia and can be hereditary, in which E-cadherin alteration plays a pivotal role. Intestinal type is more frequently observed in older patients and follows multifocal atrophic gastritis. This is usually accompanied by intestinal metaplasia and leads to cancer via dysplasia, and thus intestinal metaplasia is considered a dependable morphological marker for GC risk. Intestinal adenocarcinoma predominates in the high-risk areas whereas the diffuse adenocarcinoma is more common in low-risk areas. Discussion: Classically, genetic instability and Helicobater pylori (H. Pylori) infection are often identified in intestinal GC. The great majority of GCs are sporadic and result from the cumulative effects of different environmental risk factors; smoking, alcohol consumption and dietary habits have been addressed as significant. H. Pylori infection and proinflammatory cytokine gene polymorphisms represent other features of this compound process that leads to the development of GC. Other molecular pathway well described in GC is microsatellite instability (MSI) that related with specific clinic-pathological features. Conclusion: In this review we focused on the role of H. Pylori infection, MSI and alterations of CDH1 (E-Cadherin) gene.

Original languageEnglish
Pages (from-to)172-176
Number of pages5
JournalAnnali Italiani di Chirurgia
Volume83
Issue number3
Publication statusPublished - 2012

Fingerprint

Stomach Neoplasms
Carcinogenesis
Pylorus
Metaplasia
Neoplasms
Microsatellite Instability
Cadherins
Stomach
Adenocarcinoma
Infection
Intestinal Neoplasms
Atrophic Gastritis
Feeding Behavior
Epigenomics
Alcohol Drinking
Genes
Smoking
Cytokines
Mortality
Incidence

Keywords

  • E-cadherin
  • Gastric tumorigenesis
  • Genomic instability
  • Helicobacter pilory

ASJC Scopus subject areas

  • Surgery

Cite this

Gastric cancer carcinogenesis and tumor progression. / Corso, Giovanni; Seruca, Raquel; Roviello, Franco.

In: Annali Italiani di Chirurgia, Vol. 83, No. 3, 2012, p. 172-176.

Research output: Contribution to journalArticle

Corso, G, Seruca, R & Roviello, F 2012, 'Gastric cancer carcinogenesis and tumor progression', Annali Italiani di Chirurgia, vol. 83, no. 3, pp. 172-176.
Corso, Giovanni ; Seruca, Raquel ; Roviello, Franco. / Gastric cancer carcinogenesis and tumor progression. In: Annali Italiani di Chirurgia. 2012 ; Vol. 83, No. 3. pp. 172-176.
@article{22630aa1923f45239ef262e45be05213,
title = "Gastric cancer carcinogenesis and tumor progression",
abstract = "Background: Gastric cancer (GC) remains one of the leading causes of cancer-related deaths worldwide, even though a decline has been observed in its incidence and the mortality rate in recent decades. Gastric carcinogenesis is a complex phenomena involving multiple epigenetic and genetic factors; several genetic, environmental and infectious agents interact causing a cumulative effect in the early steps of gastric carcinogenesis. Materials and Methods: The most commonly used classifications of GC are the World Health Organization (WHO) and the Laur{\'e}n classifications which describes two main histological types, diffuse and intestinal, which have different clinicopathological characteristics. Diffuse cancer occurs more commonly in young patients, can be multifocal, is not often accompanied by intestinal metaplasia and can be hereditary, in which E-cadherin alteration plays a pivotal role. Intestinal type is more frequently observed in older patients and follows multifocal atrophic gastritis. This is usually accompanied by intestinal metaplasia and leads to cancer via dysplasia, and thus intestinal metaplasia is considered a dependable morphological marker for GC risk. Intestinal adenocarcinoma predominates in the high-risk areas whereas the diffuse adenocarcinoma is more common in low-risk areas. Discussion: Classically, genetic instability and Helicobater pylori (H. Pylori) infection are often identified in intestinal GC. The great majority of GCs are sporadic and result from the cumulative effects of different environmental risk factors; smoking, alcohol consumption and dietary habits have been addressed as significant. H. Pylori infection and proinflammatory cytokine gene polymorphisms represent other features of this compound process that leads to the development of GC. Other molecular pathway well described in GC is microsatellite instability (MSI) that related with specific clinic-pathological features. Conclusion: In this review we focused on the role of H. Pylori infection, MSI and alterations of CDH1 (E-Cadherin) gene.",
keywords = "E-cadherin, Gastric tumorigenesis, Genomic instability, Helicobacter pilory",
author = "Giovanni Corso and Raquel Seruca and Franco Roviello",
year = "2012",
language = "English",
volume = "83",
pages = "172--176",
journal = "Annali Italiani di Chirurgia",
issn = "0003-469X",
publisher = "Edizioni Luigi Pozzi S.r.l.",
number = "3",

}

TY - JOUR

T1 - Gastric cancer carcinogenesis and tumor progression

AU - Corso, Giovanni

AU - Seruca, Raquel

AU - Roviello, Franco

PY - 2012

Y1 - 2012

N2 - Background: Gastric cancer (GC) remains one of the leading causes of cancer-related deaths worldwide, even though a decline has been observed in its incidence and the mortality rate in recent decades. Gastric carcinogenesis is a complex phenomena involving multiple epigenetic and genetic factors; several genetic, environmental and infectious agents interact causing a cumulative effect in the early steps of gastric carcinogenesis. Materials and Methods: The most commonly used classifications of GC are the World Health Organization (WHO) and the Laurén classifications which describes two main histological types, diffuse and intestinal, which have different clinicopathological characteristics. Diffuse cancer occurs more commonly in young patients, can be multifocal, is not often accompanied by intestinal metaplasia and can be hereditary, in which E-cadherin alteration plays a pivotal role. Intestinal type is more frequently observed in older patients and follows multifocal atrophic gastritis. This is usually accompanied by intestinal metaplasia and leads to cancer via dysplasia, and thus intestinal metaplasia is considered a dependable morphological marker for GC risk. Intestinal adenocarcinoma predominates in the high-risk areas whereas the diffuse adenocarcinoma is more common in low-risk areas. Discussion: Classically, genetic instability and Helicobater pylori (H. Pylori) infection are often identified in intestinal GC. The great majority of GCs are sporadic and result from the cumulative effects of different environmental risk factors; smoking, alcohol consumption and dietary habits have been addressed as significant. H. Pylori infection and proinflammatory cytokine gene polymorphisms represent other features of this compound process that leads to the development of GC. Other molecular pathway well described in GC is microsatellite instability (MSI) that related with specific clinic-pathological features. Conclusion: In this review we focused on the role of H. Pylori infection, MSI and alterations of CDH1 (E-Cadherin) gene.

AB - Background: Gastric cancer (GC) remains one of the leading causes of cancer-related deaths worldwide, even though a decline has been observed in its incidence and the mortality rate in recent decades. Gastric carcinogenesis is a complex phenomena involving multiple epigenetic and genetic factors; several genetic, environmental and infectious agents interact causing a cumulative effect in the early steps of gastric carcinogenesis. Materials and Methods: The most commonly used classifications of GC are the World Health Organization (WHO) and the Laurén classifications which describes two main histological types, diffuse and intestinal, which have different clinicopathological characteristics. Diffuse cancer occurs more commonly in young patients, can be multifocal, is not often accompanied by intestinal metaplasia and can be hereditary, in which E-cadherin alteration plays a pivotal role. Intestinal type is more frequently observed in older patients and follows multifocal atrophic gastritis. This is usually accompanied by intestinal metaplasia and leads to cancer via dysplasia, and thus intestinal metaplasia is considered a dependable morphological marker for GC risk. Intestinal adenocarcinoma predominates in the high-risk areas whereas the diffuse adenocarcinoma is more common in low-risk areas. Discussion: Classically, genetic instability and Helicobater pylori (H. Pylori) infection are often identified in intestinal GC. The great majority of GCs are sporadic and result from the cumulative effects of different environmental risk factors; smoking, alcohol consumption and dietary habits have been addressed as significant. H. Pylori infection and proinflammatory cytokine gene polymorphisms represent other features of this compound process that leads to the development of GC. Other molecular pathway well described in GC is microsatellite instability (MSI) that related with specific clinic-pathological features. Conclusion: In this review we focused on the role of H. Pylori infection, MSI and alterations of CDH1 (E-Cadherin) gene.

KW - E-cadherin

KW - Gastric tumorigenesis

KW - Genomic instability

KW - Helicobacter pilory

UR - http://www.scopus.com/inward/record.url?scp=84866144479&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84866144479&partnerID=8YFLogxK

M3 - Article

VL - 83

SP - 172

EP - 176

JO - Annali Italiani di Chirurgia

JF - Annali Italiani di Chirurgia

SN - 0003-469X

IS - 3

ER -