About this Journal Submit a Manuscript Table of Contents

E-Cadherin and Solid Tumors

Call for Papers

Cadherin type 1 (CDH1) is a classical gene from the cadherin superfamily, which encodes the epithelial-cadherin (E-CADH) protein. The protein is a calcium-dependent cell-cell adhesion glycoprotein comprising five extracellular domains, a transmembrane region and a cytoplasmatic tail, the latter providing a link to the actin cytoskeleton through an association with various catenins.

Genetic E-CADH mutations are the cause of hereditary diffuse gastric cancer (HDGC), but increased data also highlight a susceptibility of E-CADH alterations with other solid tumors. Thus, E-CADH alterations could be considered as an important marker associated with several solid tumors and E-CADH alterations or its cleaved soluble form level well fits with a negative prognostic score in most of these tumors.

The current paradigm sees the acquisition of an invasive cancer phenotype associated with a loss of E-CADH during the process of epithelial mesenchymal transition (EMT), but the entire process is complex and not well understood.

In addition to genetic alterations, recent studies have focused on hypoxia, H. pylori infection, and microenvironment and epigenetic factors as agents to participate in a diffuse alteration of E-CADH expression. Some of these factors have started to be appreciated for their effects on cancer development and invasion and for having a potential role in the development of targeted therapies.

We particularly take an interest in manuscripts that report the identification of E-CADH variants and factors that influence its expression resulting in a better knowledge of E-CADH effects on cancer progression, metastasis, and EMT acquisition. Results of clinical data and trials regarding early diagnosis, prognosis, and response to tumor therapies are welcome. Moreover, E-CADH pathway target for therapies would be also of interest. Potential topics include, but are not limited to:

  • Methods for the identification of E-CADH alteration and alternative splicing measurements
  • Mechanistic aspects and effects of E-CADH alterations in different solid tumors
  • The significance of soluble E-CADH and CDH1 alterations in clinical guidance
  • New technological approaches to define the physio/pathological role of E-CADH-pathway
  • The role of hypoxia and microenvironmental and infectious agents in E-CADH expression

Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/bmri/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/bmri/genetics/cst/ according to the following timetable:

Manuscript DueFriday, 2 May, 2014
First Round of ReviewsFriday, 25 July 2014
Publication DateFriday, 19 September 2014

Lead Guest Editor

  • Valli De Re, Department of Translational Researches, Oncological Referral Center, IRCCS, National Cancer Institute, Aviano, Italy

Guest Editors