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Mutations of the DPC4/Smad4 gene in neuroendocrine pancreatic tumors.
Oncogene 1999; 18(14):2367-71O

Abstract

Tumors of the endocrine pancreas are extremely rare, and molecular mechanisms leading to their development are not well understood. A candidate tumor suppressor gene, DPC4, located at 18q21, has recently been shown to be inactivated in half of pancreatic adenocarcinoma xenografts. The close anatomical relationship of the exocrine and endocrine pancreas prompted us to determine the role of DPC4 in the tumorigenesis of 25 pancreatic islet cell tumors (11 insulinomas, nine non-functioning endocrine carcinomas, three gastrinomas, two vipomas). A mutation screening of the highly conserved COOH-terminal domain of DPC4 (exons 8-11) was performed by single-strand conformational variant (SSCP) analysis and a PCR-based deletion assay. Five of nine (55%) non-functioning endocrine pancreatic carcinomas revealed either point mutations, small intragenic deletions or homozygous deletion of DPC4 sequences compared to none of the insulinomas, gastrinomas or vipomas. These results suggest that DPC4 is an important target gene promoting tumorigenesis of non-functioning neuroendocrine pancreatic carcinomas.

Authors+Show Affiliations

Department of Surgery, Philipps-University Marburg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10327057

Citation

Bartsch, D, et al. "Mutations of the DPC4/Smad4 Gene in Neuroendocrine Pancreatic Tumors." Oncogene, vol. 18, no. 14, 1999, pp. 2367-71.
Bartsch D, Hahn SA, Danichevski KD, et al. Mutations of the DPC4/Smad4 gene in neuroendocrine pancreatic tumors. Oncogene. 1999;18(14):2367-71.
Bartsch, D., Hahn, S. A., Danichevski, K. D., Ramaswamy, A., Bastian, D., Galehdari, H., ... Rothmund, M. (1999). Mutations of the DPC4/Smad4 gene in neuroendocrine pancreatic tumors. Oncogene, 18(14), pp. 2367-71.
Bartsch D, et al. Mutations of the DPC4/Smad4 Gene in Neuroendocrine Pancreatic Tumors. Oncogene. 1999 Apr 8;18(14):2367-71. PubMed PMID: 10327057.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mutations of the DPC4/Smad4 gene in neuroendocrine pancreatic tumors. AU - Bartsch,D, AU - Hahn,S A, AU - Danichevski,K D, AU - Ramaswamy,A, AU - Bastian,D, AU - Galehdari,H, AU - Barth,P, AU - Schmiegel,W, AU - Simon,B, AU - Rothmund,M, PY - 1999/5/18/pubmed PY - 1999/5/18/medline PY - 1999/5/18/entrez SP - 2367 EP - 71 JF - Oncogene JO - Oncogene VL - 18 IS - 14 N2 - Tumors of the endocrine pancreas are extremely rare, and molecular mechanisms leading to their development are not well understood. A candidate tumor suppressor gene, DPC4, located at 18q21, has recently been shown to be inactivated in half of pancreatic adenocarcinoma xenografts. The close anatomical relationship of the exocrine and endocrine pancreas prompted us to determine the role of DPC4 in the tumorigenesis of 25 pancreatic islet cell tumors (11 insulinomas, nine non-functioning endocrine carcinomas, three gastrinomas, two vipomas). A mutation screening of the highly conserved COOH-terminal domain of DPC4 (exons 8-11) was performed by single-strand conformational variant (SSCP) analysis and a PCR-based deletion assay. Five of nine (55%) non-functioning endocrine pancreatic carcinomas revealed either point mutations, small intragenic deletions or homozygous deletion of DPC4 sequences compared to none of the insulinomas, gastrinomas or vipomas. These results suggest that DPC4 is an important target gene promoting tumorigenesis of non-functioning neuroendocrine pancreatic carcinomas. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/10327057/Mutations_of_the_DPC4/Smad4_gene_in_neuroendocrine_pancreatic_tumors_ L2 - http://dx.doi.org/10.1038/sj.onc.1202585 DB - PRIME DP - Unbound Medicine ER -