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Updated: Aug 6, 2026

Tissue Engineering of Tumor Stromal Microenvironment with Application to Cancer Cell Invasion
05:48

Tissue Engineering of Tumor Stromal Microenvironment with Application to Cancer Cell Invasion

Published on: March 18, 2014

E-cadherin as a tumor (invasion) suppressor gene

W Birchmeier1

  • 1Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|February 1, 1995
PubMed

Insights

Diffuse-type gastric carcinomas exhibit reduced cell adhesion due to E-cadherin gene mutations. These mutations disrupt calcium-binding sites, significantly contributing to cancer development and poor patient survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Diffuse-type gastric carcinomas are characterized by decreased cellular adhesion.
  • E-cadherin, a key cell adhesion molecule, is crucial for maintaining tissue integrity.

Purpose of the Study:

  • To investigate the role of E-cadherin gene mutations in diffuse-type gastric carcinomas.
  • To establish the link between E-cadherin alterations and cancer development and patient prognosis.

Main Methods:

  • Analysis of E-cadherin gene mutations in diffuse-type gastric carcinoma samples.
  • Evaluation of the impact of mutations on E-cadherin protein function, specifically calcium-binding sites.

Main Results:

  • Approximately 50% of diffuse-type gastric carcinomas harbor mutations in the E-cadherin gene.
  • These mutations lead to the destruction of critical calcium-binding sites within E-cadherin.
  • Strong in vivo evidence supports the role of E-cadherin alterations in tumorigenesis.

Conclusions:

  • Mutations in the E-cadherin gene are a significant factor in the pathogenesis of diffuse-type gastric carcinomas.
  • E-cadherin alterations are strongly associated with the development of this cancer and reduced patient survival.

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