Expression of Notch-1 and alteration of the E-cadherin/beta-catenin cell adhesion complex are observed in primary cutaneous neuroendocrine carcinoma (Merkel cell carcinoma)

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Μικρογραφία εικόνας

Ημερομηνία

Συγγραφείς

Panelos, J.
Batistatou, A.
Paglierani, M.
Zioga, A.
Maio, V.
Santi, R.
Pimpinelli, N.
De Giorgi, V.
Santucci, M.
Massi, D.

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Περίληψη

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Είδος δημοσίευσης σε συνέδριο

Είδος περιοδικού

peer-reviewed

Είδος εκπαιδευτικού υλικού

Όνομα συνεδρίου

Όνομα περιοδικού

Mod Pathol

Όνομα βιβλίου

Σειρά βιβλίου

Έκδοση βιβλίου

Συμπληρωματικός/δευτερεύων τίτλος

Περιγραφή

Increasing evidence indicates that Notch signaling contributes to physiological processes, including development and differentiation, as well as tumorigenesis, either as a tumor promoter or suppressor, depending on cellular context, expression levels and cross talk with other signaling systems. Recent studies reported absent or minimal Notch-1 expression in neuroendocrine tumors of the lung and gastrointestinal tract, suggesting a tumor-suppressor function of Notch-1. Merkel cell carcinoma is a rare and highly aggressive primary cutaneous neuroendocrine carcinoma. Because no information is available on Notch-1 expression in this tumor, we have investigated a series of 31 Merkel cell carcinoma for Notch-1 immunoreactivity. Immunoreactivities for E-cadherin and beta-catenin were also analyzed. All but 1 Merkel cell carcinoma (30 of 31) retained cytoplasmic and membrane Notch-1 expression in more than 50% of cells. beta-Catenin displayed a prevalent membrane-associated staining in 30 of 31 cases, and 22 cases showed more than 50% of immunoreactive cells whereas nuclear beta-catenin was seen only in 2 of 31 cases. E-cadherin membranous expression was remarkably low, as only 1 of 26 cases was found positive in more than 50% of cells. In contrast with neuroendocrine tumors in other tissues, evident Notch-1 expression was found in Merkel cell carcinoma. This finding does not support a tumor-suppressor function of Notch-1 in Merkel cell carcinoma. Downregulation of E-cadherin and diffuse membranous beta-catenin expression suggest a dysregulation of the E-cadherin/beta-catenin complex in Merkel cell carcinoma. This may contribute to local invasion and distant metastasis.

Περιγραφή

Λέξεις-κλειδιά

Adult, Aged, Aged, 80 and over, Cadherins/*metabolism, Carcinoid Tumor/metabolism/pathology, Carcinoma, Merkel Cell/*metabolism/mortality/secondary, Cell Adhesion, Cell Membrane/metabolism/pathology, Cytoplasm/metabolism/pathology, Down-Regulation, Female, Fluorescent Antibody Technique, Indirect, Humans, Immunoenzyme Techniques, Male, Middle Aged, Receptor, Notch1/*metabolism, Skin Neoplasms/*metabolism/mortality/pathology, Survival Rate, Tumor Markers, Biological/metabolism, beta Catenin/*metabolism

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Σύνδεσμος

http://www.ncbi.nlm.nih.gov/pubmed/19396152
http://www.nature.com/modpathol/journal/v22/n7/pdf/modpathol200955a.pdf

Γλώσσα

en

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Γενική Περιγραφή / Σχόλια

Ίδρυμα και Σχολή/Τμήμα του υποβάλλοντος

Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής

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Χορηγός

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