TY - JOUR
T1 - Allelic alterations in pancreatic endocrine tumors identified by genome-wide single nucleotide polymorphism analysis
AU - Nagano, Yasuhiko
AU - Do, Ha Kim
AU - Zhang, Li
AU - White, Jill A.
AU - Yao, James C.
AU - Hamilton, Stanley R.
AU - Rashid, Asif
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2007/6
Y1 - 2007/6
N2 - Pancreatic endocrine tumors (PETs) are uncommon and the genetic alterations in these indolent tumors are not well characterized. Chromosomal imbalances are frequent in tumors but PETs have not been studied by high-density single nucleotide polymorphism (SNP) array. We used genome-wide high-density SNP array analysis to detect copy number alterations using matched tumor and non-neoplastic tissue samples from 15 patients with PETs. In our study, whole or partial loss of chromosomes 1, 3, 11, 22 was present in 40, 47, 53, 40% of tumors respectively, and gain of chromosomes 5, 7, 12, 14, 17, and 20 was present in 47, 60, 47, 53, 53, and 47% of tumors respectively. One tumor had loss of heterozygosity of chromosome 3 and another of chromosome 22 without copy number alterations, suggesting uniparental disomy due to non-disjunction and deletion or to chromosomal recombination. Chromosomal aberrations of the autosomal chromosomes were correlated with chromosomal loss or gain of other chromosomes (r>0.5, P<0.5). About 60% of PETs had high allelic imbalances (AI) defined by more than four chromosomal aberrations, and 40% of tumors had low AI. The PETs with high AI were larger: the mean tumor size with high AI was 5.4 ± 3.1 cm compared with 2.3 ± 1.3 cm for low AI (P=0.03). Our study shows that genome-wide allelotyping is a powerful new tool for the analysis of AI in PETs.
AB - Pancreatic endocrine tumors (PETs) are uncommon and the genetic alterations in these indolent tumors are not well characterized. Chromosomal imbalances are frequent in tumors but PETs have not been studied by high-density single nucleotide polymorphism (SNP) array. We used genome-wide high-density SNP array analysis to detect copy number alterations using matched tumor and non-neoplastic tissue samples from 15 patients with PETs. In our study, whole or partial loss of chromosomes 1, 3, 11, 22 was present in 40, 47, 53, 40% of tumors respectively, and gain of chromosomes 5, 7, 12, 14, 17, and 20 was present in 47, 60, 47, 53, 53, and 47% of tumors respectively. One tumor had loss of heterozygosity of chromosome 3 and another of chromosome 22 without copy number alterations, suggesting uniparental disomy due to non-disjunction and deletion or to chromosomal recombination. Chromosomal aberrations of the autosomal chromosomes were correlated with chromosomal loss or gain of other chromosomes (r>0.5, P<0.5). About 60% of PETs had high allelic imbalances (AI) defined by more than four chromosomal aberrations, and 40% of tumors had low AI. The PETs with high AI were larger: the mean tumor size with high AI was 5.4 ± 3.1 cm compared with 2.3 ± 1.3 cm for low AI (P=0.03). Our study shows that genome-wide allelotyping is a powerful new tool for the analysis of AI in PETs.
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U2 - 10.1677/ERC-06-0090
DO - 10.1677/ERC-06-0090
M3 - Article
C2 - 17639061
AN - SCOPUS:34547803711
SN - 1351-0088
VL - 14
SP - 483
EP - 492
JO - Endocrine-related cancer
JF - Endocrine-related cancer
IS - 2
ER -