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[Gastrin cell hyperplasia associated with duodenal MEN1-related gastrinomas: histopathology and genetics].
Verh Dtsch Ges Pathol. 2007; 91:320-9.VD

Abstract

AIMS

The identification of precursor lesions has a great impact on our understanding of tumorigenesis. In this study we investigated whether preneoplastic lesions can be identified in sporadic gastrinomas and in gastrinomas in multiple endocrine neoplasia type 1 (MEN1) patients. These lesions were tested for loss of heterozygosity (LOH) of the MEN1 gene locus on chromosome 11q13.

MATERIAL AND METHODS

Tissue specimens from 25 patients with Zollinger-Ellison syndrome (ZES) were analyzed. The MEN1 status was assessed clinically and by mutational analysis. For simultaneous analysis of hormones and allelic deletions a combined FISH fluorescence in situ hybridization/immunofluorescence protocol was established.

RESULTS

Hyperplastic gastrin cell lesions were present in the nontumorous mucosa of all MEN1 patients, but not in 12 patients with sporadic duodenal gastrinomas. The hyperplastic gastrin cells retained both 11q13 alleles. 11q13 LOH was, however, detected in duodenal gastrinomas, some as small as 300 microm in diameter, in 13 patients with MEN1.

CONCLUSIONS

MEN1-associated duodenal gastrinomas, but not sporadic gastrinomas, are associated with gastrin cell hyperplasia. It is therefore likely that hyperplastic gastrin cell lesions precede the development of MEN1-associated duodenal gastrinomas. Allelic deletion of the MEN1 gene locus may reflect a decisive initial event in the development of multifocal MEN1-associated gastrinomas from hyperplastic gastrin cell lesions.

Authors+Show Affiliations

Institut für Pathologie, Universitätsklinikum S-H, Campus Kiel.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

ger

PubMed ID

18314630

Citation

Anlauf, M, et al. "[Gastrin Cell Hyperplasia Associated With Duodenal MEN1-related Gastrinomas: Histopathology and Genetics]." Verhandlungen Der Deutschen Gesellschaft Fur Pathologie, vol. 91, 2007, pp. 320-9.
Anlauf M, Perren A, Klöppel G. [Gastrin cell hyperplasia associated with duodenal MEN1-related gastrinomas: histopathology and genetics]. Verh Dtsch Ges Pathol. 2007;91:320-9.
Anlauf, M., Perren, A., & Klöppel, G. (2007). [Gastrin cell hyperplasia associated with duodenal MEN1-related gastrinomas: histopathology and genetics]. Verhandlungen Der Deutschen Gesellschaft Fur Pathologie, 91, 320-9.
Anlauf M, Perren A, Klöppel G. [Gastrin Cell Hyperplasia Associated With Duodenal MEN1-related Gastrinomas: Histopathology and Genetics]. Verh Dtsch Ges Pathol. 2007;91:320-9. PubMed PMID: 18314630.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Gastrin cell hyperplasia associated with duodenal MEN1-related gastrinomas: histopathology and genetics]. AU - Anlauf,M, AU - Perren,A, AU - Klöppel,G, PY - 2008/3/5/pubmed PY - 2008/4/30/medline PY - 2008/3/5/entrez SP - 320 EP - 9 JF - Verhandlungen der Deutschen Gesellschaft fur Pathologie JO - Verh Dtsch Ges Pathol VL - 91 N2 - AIMS: The identification of precursor lesions has a great impact on our understanding of tumorigenesis. In this study we investigated whether preneoplastic lesions can be identified in sporadic gastrinomas and in gastrinomas in multiple endocrine neoplasia type 1 (MEN1) patients. These lesions were tested for loss of heterozygosity (LOH) of the MEN1 gene locus on chromosome 11q13. MATERIAL AND METHODS: Tissue specimens from 25 patients with Zollinger-Ellison syndrome (ZES) were analyzed. The MEN1 status was assessed clinically and by mutational analysis. For simultaneous analysis of hormones and allelic deletions a combined FISH fluorescence in situ hybridization/immunofluorescence protocol was established. RESULTS: Hyperplastic gastrin cell lesions were present in the nontumorous mucosa of all MEN1 patients, but not in 12 patients with sporadic duodenal gastrinomas. The hyperplastic gastrin cells retained both 11q13 alleles. 11q13 LOH was, however, detected in duodenal gastrinomas, some as small as 300 microm in diameter, in 13 patients with MEN1. CONCLUSIONS: MEN1-associated duodenal gastrinomas, but not sporadic gastrinomas, are associated with gastrin cell hyperplasia. It is therefore likely that hyperplastic gastrin cell lesions precede the development of MEN1-associated duodenal gastrinomas. Allelic deletion of the MEN1 gene locus may reflect a decisive initial event in the development of multifocal MEN1-associated gastrinomas from hyperplastic gastrin cell lesions. SN - 0070-4113 UR - https://www.unboundmedicine.com/medline/citation/18314630/[Gastrin_cell_hyperplasia_associated_with_duodenal_MEN1_related_gastrinomas:_histopathology_and_genetics]_ L2 - https://medlineplus.gov/intestinalcancer.html DB - PRIME DP - Unbound Medicine ER -