Pancreatic endocrine tumors with loss of heterozygosity at the multiple endocrine neoplasia type I locus

Patricia J. Eubanks, Mark P. Sawicki, Ghasan J. Samara, Yu-Jui Yvonne Wan, Richard A. Gatti, Michael Hurwitz, Edward Passaro

Research output: Contribution to journalArticle

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Abstract

BACKGROUND: Loss of heterozygosity (LOH) at chromosome 11q13 has been demonstrated in multiple endocrine neoplasia type I (MEN I) and sporadic parathyroid tumors, pituitary adenomas, and a few types of pancreatic endocrine tumors. Gastrinomas are the most common pancreatic endocrine tumor in MEN I. We hypothesized that all pancreatic endocrine tumors have LOH at 11q13, resulting in inactivation of the previously described tumor suppressor gene in this region. METHODS: We analyzed a sporadic gastrinoma, a MEN I- associated gastrinoma, and a nonfunctional pancreatic endocrine tumor from a patient with Von Hippel-Lindau (VHL) disease for LOH at seven loci at 11q13; D11S149, PYGM, D11S427, D11S546, SEA, D11S97, and D11S146. RESULTS AND CONCLUSIONS: We found LOH at 11q13 in all three tumors. The MEN I-associated gastrinoma we analyzed is the first tumor of this type to have LOH. This is also the first report of LOH at 11q13 in a pancreatic endocrine tumor from a patient with VHL. These findings suggest that the etiology of pancreatic endocrine tumor formation involves a common genetic pathway for sporadic, MEN I, and VHL tumors.

Original languageEnglish (US)
Pages (from-to)518-520
Number of pages3
JournalAmerican Journal of Surgery
Volume173
Issue number6
DOIs
StatePublished - Jun 1997

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Multiple Endocrine Neoplasia Type 1
Loss of Heterozygosity
Gastrinoma
Neoplasms
von Hippel-Lindau Disease
Pituitary Neoplasms
Tumor Suppressor Genes
Chromosomes

ASJC Scopus subject areas

  • Surgery

Cite this

Pancreatic endocrine tumors with loss of heterozygosity at the multiple endocrine neoplasia type I locus. / Eubanks, Patricia J.; Sawicki, Mark P.; Samara, Ghasan J.; Wan, Yu-Jui Yvonne; Gatti, Richard A.; Hurwitz, Michael; Passaro, Edward.

In: American Journal of Surgery, Vol. 173, No. 6, 06.1997, p. 518-520.

Research output: Contribution to journalArticle

Eubanks, Patricia J. ; Sawicki, Mark P. ; Samara, Ghasan J. ; Wan, Yu-Jui Yvonne ; Gatti, Richard A. ; Hurwitz, Michael ; Passaro, Edward. / Pancreatic endocrine tumors with loss of heterozygosity at the multiple endocrine neoplasia type I locus. In: American Journal of Surgery. 1997 ; Vol. 173, No. 6. pp. 518-520.
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abstract = "BACKGROUND: Loss of heterozygosity (LOH) at chromosome 11q13 has been demonstrated in multiple endocrine neoplasia type I (MEN I) and sporadic parathyroid tumors, pituitary adenomas, and a few types of pancreatic endocrine tumors. Gastrinomas are the most common pancreatic endocrine tumor in MEN I. We hypothesized that all pancreatic endocrine tumors have LOH at 11q13, resulting in inactivation of the previously described tumor suppressor gene in this region. METHODS: We analyzed a sporadic gastrinoma, a MEN I- associated gastrinoma, and a nonfunctional pancreatic endocrine tumor from a patient with Von Hippel-Lindau (VHL) disease for LOH at seven loci at 11q13; D11S149, PYGM, D11S427, D11S546, SEA, D11S97, and D11S146. RESULTS AND CONCLUSIONS: We found LOH at 11q13 in all three tumors. The MEN I-associated gastrinoma we analyzed is the first tumor of this type to have LOH. This is also the first report of LOH at 11q13 in a pancreatic endocrine tumor from a patient with VHL. These findings suggest that the etiology of pancreatic endocrine tumor formation involves a common genetic pathway for sporadic, MEN I, and VHL tumors.",
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AU - Eubanks, Patricia J.

AU - Sawicki, Mark P.

AU - Samara, Ghasan J.

AU - Wan, Yu-Jui Yvonne

AU - Gatti, Richard A.

AU - Hurwitz, Michael

AU - Passaro, Edward

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AB - BACKGROUND: Loss of heterozygosity (LOH) at chromosome 11q13 has been demonstrated in multiple endocrine neoplasia type I (MEN I) and sporadic parathyroid tumors, pituitary adenomas, and a few types of pancreatic endocrine tumors. Gastrinomas are the most common pancreatic endocrine tumor in MEN I. We hypothesized that all pancreatic endocrine tumors have LOH at 11q13, resulting in inactivation of the previously described tumor suppressor gene in this region. METHODS: We analyzed a sporadic gastrinoma, a MEN I- associated gastrinoma, and a nonfunctional pancreatic endocrine tumor from a patient with Von Hippel-Lindau (VHL) disease for LOH at seven loci at 11q13; D11S149, PYGM, D11S427, D11S546, SEA, D11S97, and D11S146. RESULTS AND CONCLUSIONS: We found LOH at 11q13 in all three tumors. The MEN I-associated gastrinoma we analyzed is the first tumor of this type to have LOH. This is also the first report of LOH at 11q13 in a pancreatic endocrine tumor from a patient with VHL. These findings suggest that the etiology of pancreatic endocrine tumor formation involves a common genetic pathway for sporadic, MEN I, and VHL tumors.

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