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Literature DB >> 12114764

Origin and Genetic Background of Insulinomas.

G. Rindi¹, M. E. Candusso, A. L. Marchetti.
1. MD, PHD.

Abstract

Insulin-producing B cell tumors (insulinomas) are the most frequent functioning endocrine tumors of the pancreas. Available experimental evidence suggests that the islet B cell is the most likely cell of origin of insulinomas, while the duct endocrine cell should be considered if rearrangement of the pancreatic parenchyma occurs. Data on the genetic background of insulinomas suggest that the B cell tumor development may result from alteration of several genes, including the multiple endocrine neoplasia type 1 (MEN1) gene.

Entities: Disease Gene

Year: 1999 PMID： 12114764 DOI： 10.1007/bf02739770

Source DB: PubMed Journal: Endocr Pathol ISSN： 1046-3976 Impact factor: 3.943

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References

59 in total

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Journal: J Exp Med Date: 1992-12-01 Impact factor: 14.307

Origin and Genetic Background of Insulinomas.

1. Identification of a transcriptional enhancer important for enteroendocrine and pancreatic islet cell-specific expression of the secretin gene.

2. Allelic deletions on chromosome 11q13 in multiple endocrine neoplasia type 1-associated and sporadic gastrinomas and pancreatic endocrine tumors.

3. Loss of heterozygosity studies at the retinoblastoma and breast cancer susceptibility (BRCA2) loci in pituitary, parathyroid, pancreatic and carcinoid tumours.

4. Differential gastrin gene expression in rat gastrointestinal tract and pancreas during neonatal development.

5. Histologic, immunofluorescence, and ultrastructural study of malignant islet-cell tumors of the pancreas induced in hamsters by BK human papovavirus.

6. Role of p53 tumor suppressor gene in pancreatic endocrine tumors of Chinese patients.

Review 7. Multiple steps in carcinogenesis involving alterations of multiple tumor suppressor genes.

8. Mutation of the MENIN gene in sporadic pancreatic endocrine tumors.

9. Transitional cells in the regenerating pancreas.

10. Expression of a tumor necrosis factor alpha transgene in murine pancreatic beta cells results in severe and permanent insulitis without evolution towards diabetes.