COMPARATIVE GENOMIC HYBRIDIZATION ANALYSIS OF SPORADIC NEUROENDOCRINETUMORS OF THE DIGESTIVE-SYSTEM

Little information is available on the molecular mechanisms underlying neuroendocrine tumorigenesis. To obtain an overview of the genomic im balances characterizing these tumors, we studied 20 benign or malignan t sporadic endocrine gastroenteropancreatic tumors by comparative geno mic hybridization. Chromosomal imbalances were found in all rumors. Ga ins of chromosomal material were more frequent than losses, The most f requent gains were of chromosomes and chromosome arms 5 (55%), 14 (55% ), 17q (55%), and 7 (50%). Losses were most frequent from 11q (30%) an d 16p (30%). Gains of chromosome 5 did not occur in nonmetastatic tumo rs, whereas losses of 9p were observed exclusively in intestinal tumor s. In addition, we found two high-level amplifications, of 17q11-21 an d 19q13. A complementary FISH analysis revealed that the gain in 17q11 -21 included amplification of the protooncogene HER2/neu. As in multip le endocrine neoplasia type-I-associated tumors, deletions of chromoso me band 11q13 appear to be involved in the development of sporadic dig estive tract neuroendocrine tumors, but our results suggest that other chromosomal regions are also involved. (C) 1998 Wiley-Liss, Inc.