This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Saggiorato, E. Articles by Volante, M. Search for Related Content PubMed Articles by Saggiorato, E. Articles by Volante, M.

JMD 2007, Vol. 9, No. 2
Copyright © 2007 American Society for Investigative Pathology & Association for Molecular Pathology

Absence of RET Gene Point Mutations in Sporadic Thyroid C-Cell Hyperplasia

Enrico Saggiorato^*, Ida Rapa, Francesca Garino^*, Gianni Bussolati, Fabio Orlandi^*, Mauro Papotti and Marco Volante

From the Section of Endocrinology, * the Department of Clinical and Biological Sciences, Division of Pathology, and the Department of Biomedical Sciences and Oncology, Division of Pathology, University of Turin, Turin, Italy

Progression from C-cell hyperplasia (CCH) to medullary thyroid carcinoma (MTC) has been demonstrated to date only in familial forms, whereas in nonfamilial MTC, such hypothesis is suggested by the rare concurrence of both lesions, although no epidemiological and molecular data are available to prove or disprove this event. Therefore, the clinical management of patients with sporadic CCH is controversial. To evaluate the malignant potential of sporadic CCHs, pure laser-microdissected C-cell populations of 24 CCH cases, either reactive or associated with nonfamilial MTC, were analyzed for MTC-associated protein neural cell adhesion molecule expression and RET point mutations in exons 10, 11, 15, and 16, by using immunohistochemistry and polymerase chain reaction-single-strand conformation polymorphism/heteroduplex electrophoresis/direct sequencing, respectively. No RET mutations were found in any of the 24 CCH cases, whereas M918T mutation was detected in three concomitant MTCs. Neural cell adhesion molecule was immunoreactive in the majority of CCH associated with MTC even in the absence of morphological atypia, but not in reactive forms. The absence of RET alterations in all cases of CCH examined supports the hypothesis that the development of MTC is independent of pre-existing CCH in the nonfamilial setting; thus, sporadic CCH should not be considered a risk factor for nonfamilial MTC.

This article has been cited by other articles:

				L Foppiani, F Forzano, I Ceccherini, W Bruno, P Ghiorzo, F Caroli, P Quilici, R Bandelloni, A Arlandini, G Sartini, et al. Uncommon association of germline mutations of RET proto-oncogene and CDKN2A gene Eur. J. Endocrinol., March 1, 2008; 158(3): 417 - 422. [Abstract] [Full Text] [PDF]