The first two authors contributed equally to this work.
Chromosome 18 deletions are common events in classical midgut carcinoid tumors
Article first published online: 3 APR 2001
Copyright © 2001 Wiley-Liss, Inc.
International Journal of Cancer
Volume 92, Issue 6, pages 812–815, 15 June 2001
How to Cite
Löllgen, R.-M., Hessman, O., Szabo, E., Westin, G. and Åkerström, G. (2001), Chromosome 18 deletions are common events in classical midgut carcinoid tumors. Int. J. Cancer, 92: 812–815. doi: 10.1002/ijc.1276
- Issue published online: 3 MAY 2001
- Article first published online: 3 APR 2001
- Manuscript Accepted: 19 JAN 2001
- Manuscript Revised: 15 DEC 2000
- Manuscript Received: 30 OCT 2000
- Swedish Medical Research Council
- Swedish Cancer Society
- Lions Fund for Cancer Research
- Swedish Society of Medicine
- Erik, Karin and Gösta Selanders Foundation
- Swedish Society for Medical Research
- loss of heterozygosity;
- chromosome 18;
- carcinoid tumor;
Classical midgut carcinoids are rare intestinal neuroendocrine tumors that often present with metastases at diagnosis. In contrast to foregut carcinoids, midgut carcinoids are not related to the multiple endocrine neoplasia type 1 syndrome, and the mechanisms involved in their tumorigenesis are unknown. Eight classical midgut carcinoids were analyzed by genome-wide screening for loss of heterozygosity. Deletions on chromosome 18 were found in 88% of the tumors. DNA sequencing and immunohistochemical staining for Smad4/DPC4, which often is homozygously mutated in pancreatic and colon carcinomas, revealed no aberrations. In 1 tumor, a region telomeric to the Smad4/DPC4/DCC genes at 18q21 was deleted. Other chromosomes were affected in 3 lesions only. The high frequency of chromosome 18 deletions strongly indicates a genetic alteration of importance in classical midgut carcinoid tumorigenesis, apparently not involving the Smad4/DPC4 gene. © 2001 Wiley-Liss, Inc.