Genetic susceptibility to gastric carcinoma

• Type: Article in International Scientific Journal
• Date: 2007

Authors

Canedo, P (Author) Other; Machado JC (Author) FMUP

Journal

Title: Acta Endoscopica

Vol. 37

Pages: 239-247

ISSN: 0240-642X

Publisher: Springer

Indexing

ISI Web of Knowledge - 0 Citations

Scopus - 1 Citation

Other information

Authenticus ID: P-004-C9X

DOI: 10.1007/bf02961793

Abstract (EN): Gastric carcinoma (GC) is the second leading cause of cancer-related death in the world, with an estimated 880,000 new cases and 650,000 deaths each year. The understanding, even if partial, of the molecular and genetic mechanisms that underlie cancer initiation and progression may become an extremely fruitful source of new and innovative approaches to cancer prevention, detection and treatment. Germline mutations of the tumour suppressor gene CDH1 that codes for the cell adhesion molecule E-cadherin, are the cause of the hereditary diffuse GC (HDGC) syndrome. Families carrying CDH1 mutations have a high incidence of diffuse GC, usually in young individuals (less than 45 years of age). Although rare (less than 2% of all GCs tire of hereditary nature), the identification of such mutations is proving invaluable in the clinical management of such families and in GC prevention in CDH1 mutation carriers. In the setting of sporadic-type GC (which constitutes about 98% of all GCs) it has been shown that individuals infected with Helicobacter pylori, a stomach colonizing bacteria, have an increased risk of developing GC H. pylori infection is now recognized as the most important risk factor for the development of sporadic GC Recently, it has also been demonstrated that H. pylori eradication has the potential to prevent GC, and that to attain the goal of prevention H. pylori eradication should be performed as soon as possible.

Language: French

Type (Professor's evaluation): Scientific

No. of pages: 9