Clinical implication of E-cadherin deficiency in lobular breast cancer

  • Giovanni CorsoEmail author
  • Gabriella Pravettoni
  • Viviana Galimberti
  • Paolo Veronesi
Letter to the Editor

We read with high interest the recent results published by Teo and Colleagues [1].

E-cadherin plays a crucial role in the maintenance of epithelial cell polarization; the deficiency of this molecule is responsible of cancer metastasis due to the loss of the cell–cell adhesion, with a concomitant increased cell motility that causes spreading in blood and lymphatic vessels [2].

Also, E-cadherin is considered an invasion suppressor, and its deregulation is often found in advanced cases of some epithelial carcinoma [3].

The mechanisms of somatic E-cadherin inactivation are multiple and controversial. In human gastric cancer with diffuse histotype, the frequency of E-cadherin somatic mutations is between 3% and greater than 50%. Loss of heterozygosis at the CDH1 locus (the gene that encodes of E-cadherin protein) ranges from 11 to 46%. Epigenetic silencing through CDH1promoter hypermethylation has been reported in frequencies that vary from 50 to 83%. Patients affected by primary gastric...



This manuscript was supported by the Italian Ministry of Health (Project Code: GR-2016-02361655. “Understanding how CDH1 germline mutations affect hereditary lobular breast cancer”).

Compliance with ethical standards

Conflict of interest

The authors declare no competing interests.

Informed consent

Not necessary for this study.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Division of Breast SurgeryEuropean Institute of Oncology IRCCSMilanItaly
  2. 2.Department of Oncology and Onco-Hematology, Faculty of MedicineUniversity of MilanMilanItaly
  3. 3.Applied Research Division for Cognitive and Psychological ScienceEuropean Institute of OncologyMilanItaly

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