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Chromosomal alterations in human pancreatic endocrine tumors
Author(s) -
Stumpf Erik,
Aalto Yan,
Höög Anders,
Kjellman Magnus,
Otonkoski Timo,
Knuutila Sakari,
Andersson Leif C.
Publication year - 2000
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1011>3.0.co;2-z
Subject(s) - comparative genomic hybridization , biology , carcinogenesis , chromosome , pancreas , gene , endocrine system , genomic dna , cancer research , neuroendocrine tumors , genetics , microbiology and biotechnology , hormone , endocrinology
Comparative genomic hybridization (CGH) was used to investigate changes in DNA copy numbers in 25 paraffin‐embedded samples of pancreatic endocrine tumors from 23 patients. Insulin was the dominant hormone in 12, glucagon in 7, somatostatin in 1, and pancreatic polypeptide in 2 tumors. One to 15 (mean, 8.1) changes in DNA copy numbers were observed in 22 of the 25 tumors. The most recurrent aberration, found in 68% of the tumors, involved gains in chromosome 7 with a minimal overlapping region at 7q11.2. Other frequent gains included chromosomes 19 (60%) and 14 (56%). Chromosome arm 20q was amplified in 48% of the cases with the minimal overlapping region of 20q11.1–13.1. The two most frequent DNA losses were found at 11q21–22 in 32% and at 11p13–15 in 24% of the cases. The amplified chromosomal regions contain several candidate genes that may be involved in islet cell tumorigenesis. The regions with most frequent losses are likely to contain still uncharacterized tumor suppressor genes. Genes Chromosomes Cancer 29:83–87, 2000. © 2000 Wiley‐Liss, Inc.