Eur J Endocrinol
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

DOI: 10.1530/eje.0.1400573
European Journal of Endocrinology, Vol 140, Issue 6, 573-576
Copyright © 1999 by European Society of Endocrinology
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Poncin, J
Right arrow Articles by Beckers, A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Poncin, J
Right arrow Articles by Beckers, A
Articles

Somatic MEN1 gene mutation does not contribute significantly to sporadic pituitary tumorigenesis

J Poncin, A Stevenaert, and A Beckers

Department of Medical Genetics, University Hospital, University of Liege, 4000 Liege, Belgium.

Pituitary adenomas are a common manifestation of multiple endocrine neoplasia type 1 (MEN1) but most of them occur sporadically. There are only a few well defined genetic abnormalities known to occur in these sporadic tumours. The MEN1 gene located on 11q13 has recently been cloned and allelic deletion and mutation analysis studies have implicated the MEN1 gene in a significant fraction of the sporadic counterparts of typical MEN1 neoplasms (parathyroid tumours, insulinomas and gastrinomas). To determine if MEN1 gene inactivation is also involved in the development of sporadic pituitary adenomas, allelic deletions of chromosome 11q13 and MEN1 gene mutations and polymorphisms were assessed in 35 sporadic tumours of the anterior pituitary (9 prolactin-secreting, 8 GH-secreting, 3 TSH-secreting, 2 TSH/GH-secreting, 4 Cushing, 9 silent). Thirty-one tumours were found to be heterozygous for at least one MEN1 intragenic polymorphism (25 cases) or for a flanking gene polymorphism (6 cases). The remaining tumours were not informative. No mutations were found in any tumour except in one prolactinoma which was homozygous or hemizygous for a mutation (1-117 C-->T) in a region close to the promoter. Unfortunately, blood or normal tissue was not available in this case. Our data show that somatic MEN1 mutations do not contribute significantly to tumorigenesis of sporadic pituitary adenomas and suggest that mutation of other genes are likely to contribute to the pathogenesis of these tumours.


This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
A. Barlier, J.-F. Vanbellinghen, A. F. Daly, M. Silvy, M.-L. Jaffrain-Rea, J. Trouillas, G. Tamagno, L. Cazabat, V. Bours, T. Brue, et al.
Mutations in the Aryl Hydrocarbon Receptor Interacting Protein Gene Are Not Highly Prevalent among Subjects with Sporadic Pituitary Adenomas
J. Clin. Endocrinol. Metab., May 1, 2007; 92(5): 1952 - 1955.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
A. Karhu and L. A. Aaltonen
Susceptibility to pituitary neoplasia related to MEN-1, CDKN1B and AIP mutations: an update
Hum. Mol. Genet., April 15, 2007; 16(R1): R73 - R79.
[Abstract] [Full Text] [PDF]

Home page
 Eur J EndocrinolHome page
A. Gurlek, N. Karavitaki, O. Ansorge, and J. A H Wass
What are the markers of aggressiveness in prolactinomas? Changes in cell biology, extracellular matrix components, angiogenesis and genetics
Eur. J. Endocrinol., February 1, 2007; 156(2): 143 - 153.
[Abstract] [Full Text] [PDF]

Home page
 Exp. Biol. Med.Home page
A. Lania, G. Mantovani, and A. Spada
Genetics of Pituitary Tumors: Focus on G-Protein Mutations
Experimental Biology and Medicine, October 1, 2003; 228(9): 1004 - 1017.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 European Society of Endocrinology.