HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Free Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Malaguarnera, R Articles by Frasca, F Search for Related Content PubMed PubMed Citation Articles by Malaguarnera, R Articles by Frasca, F

Endocrinologia, Dipartimento di Medicina Interna e Medicina Specialistica, Università di Catania, PO Garibaldi Nesima, Via Palermo 636, 95122 Catania, Italy

(Requests for offprints should be addressed to R Vigneri; Email: vigneri{at}unict.it)

At variance with other human malignancies, p53 mutations are not frequent in thyroid cancer and are believed to be responsible mainly for cancer progression to poorly differentiated and aggressive phenotype. p63 and p73, two proteins with a high degree of homology with p53, are overexpressed in thyroid cancer, but their role in cancer initiation or progression is controversial. Regulation of p53 family protein function depends on: (1) the balance between the expression of transcriptionally active (p53, TAp63, and TAp73) and inactive isoforms (Np63 and Np73); (2) their interaction and competition at DNA-responsive elements; (3) their interaction with regulatory proteins, either inhibitory or activating. In thyroid cancer, therefore, although mutations of the p53 oncosuppressor protein family are rare, other mechanisms are present, including aberrant expression of p53 family dominant negative isoforms, up-regulation of inhibitory proteins, and functional inhibition of activating proteins. The overall result is a defective oncosuppressor activity. These inactivating mechanisms may be present in the early stages of thyroid cancer and in different cancer histotypes. A better understanding of this complex network may not only ameliorate our comprehension of cancer biology, but also open the possibility of innovative diagnostic procedures and the development of targeted therapies.

This article has been cited by other articles:

				G. Salvatore, T. C. Nappi, P. Salerno, Y. Jiang, C. Garbi, C. Ugolini, P. Miccoli, F. Basolo, M. D. Castellone, A. M. Cirafici, et al. A Cell Proliferation and Chromosomal Instability Signature in Anaplastic Thyroid Carcinoma Cancer Res., November 1, 2007; 67(21): 10148 - 10158. [Abstract] [Full Text] [PDF]