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


     

DOI: 10.1530/eje.0.1470507
European Journal of Endocrinology, Vol 147, Issue 4, 507-513
Copyright © 2002 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 Wild, A
Right arrow Articles by Bartsch, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wild, A
Right arrow Articles by Bartsch, D.
Articles

Chromosome 22q in pancreatic endocrine tumors: identification of a homozygous deletion and potential prognostic associations of allelic deletions

A Wild, P Langer, I Celik, B Chaloupka, and DK Bartsch

Department of General Surgery, Philipps-University of Marburg, Baldingerstrasse, Marburg/Lahn 35043, Germany.

OBJECTIVE: A variety of human tumors frequently show allelic deletions of chromosome 22q, suggesting that inactivation of one or more tumor suppressor genes in this region is important for their tumorigenesis. METHODS: In this study, 23 patients with pancreatic endocrine tumors (PETs), including gastrinomas, VIPomas and non-functioning islet cell carcinomas, were analyzed for loss of heterozygosity (LOH) on chromosome 22q with 12 microsatellite and 7 sequence tagged site markers. RESULTS: LOH on chromosome 22q was identified in 22 of 23 (96%) PETs. Markers in the chromosomal region 22q12.1 revealed LOH rates up to 85%. Notably, one tumor revealed a homozygous deletion in a second region at 22q12.3. LOH at this locus occurred more frequently in tumors with distant metastases (10 of 11) compared with tumors without distant metastases (3 of 12; P=0.0057) and, overall, allelic loss of 22q is positively correlated with distant metastases (r=0.78; P<0.0001). CONCLUSIONS: These findings are suggestive for novel tumor suppressor gene loci at chromosome 22q that might contribute to the pathogenesis of PETs, especially to the development of distant metastases.


This article has been cited by other articles:


Home page
 Cancer Res.Home page
P. Pallante, A. Federico, M. T. Berlingieri, M. Bianco, A. Ferraro, F. Forzati, A. Iaccarino, M. Russo, G. M. Pierantoni, V. Leone, et al.
Loss of the CBX7 Gene Expression Correlates with a Highly Malignant Phenotype in Thyroid Cancer
Cancer Res., August 15, 2008; 68(16): 6770 - 6778.
[Abstract] [Full Text] [PDF]

Home page
 Endocr Relat CancerHome page
T. R Halfdanarson, J. Rubin, M. B Farnell, C. S Grant, and G. M Petersen
Pancreatic endocrine neoplasms: epidemiology and prognosis of pancreatic endocrine tumors
Endocr. Relat. Cancer, June 1, 2008; 15(2): 409 - 427.
[Abstract] [Full Text] [PDF]

Home page
 Endocr Relat CancerHome page
Y M H Jonkers, S M H Claessen, A Perren, S Schmid, P Komminoth, A A Verhofstad, L J Hofland, R R de Krijger, P J Slootweg, F C S Ramaekers, et al.
Chromosomal instability predicts metastatic disease in patients with insulinomas
Endocr. Relat. Cancer, June 1, 2005; 12(2): 435 - 447.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2002 European Society of Endocrinology.