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Clinical implication of E-cadherin deficiency in lobular breast cancer

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

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...

Notes

Acknowledgements

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.

References

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© 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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