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a Universitätsklinikum
Charité der Humboldt-Universität zu Berlin, Campus
Virchow-Klinikum, Institut für Humangenetik, Augustenburger Platz 1, D-13353 Berlin, Germany, b Universitätsklinikum Charité der
Humboldt-Universität zu Berlin, Campus Virchow-Klinikum, Medizinische
Klinik mit Schwerpunkt Hepatologie und Gastroenterologie,
Augustenburger Platz 1, D-13353 Berlin, Germany, c Max-Planck-Institut für Molekulare Genetik,
Ihnestra
e 73, D-14195 Berlin, Germany
Correspondence to: Professor B Wiedenmann. bertram.wiedenmann{at}charite.de
Accepted for publication 31 October 2000
BACKGROUND
Chromosomal
instability is observed in a wide spectrum of human cancer syndromes.
However, to date, little is known of the characteristic genetic changes
in sporadic neuroendocrine tumours of the gastroenteropancreatic system.
AIMS AND METHODWe
have studied copy number aberrations (CNAs) in 26 sporadic
neuroendocrine tumours of the enteropancreatic system (12 foregut and
14 midgut tumours) by comparative genomic hybridisation (CGH), allowing
simultaneous evaluation of the entire tumour genome.
RESULTSNearly all
tumours (25/26; that is, 96%) showed chromosomal imbalances, including
full chromosomal aneuploidies, losses and gains of chromosome arms,
interstitial deletions, and amplifications. Whereas gains of
chromosomes 4, 5, and 19 were found in both foregut and midgut tumours,
gains of chromosomes 20q (58%), 19 (50%), as well as 17p (50%), and
partial losses of chromosomes 1p (42%), 2q (42%), 3p, 4q, and 6q
(25% each) were frequently observed only in foregut tumours. In
contrast, midgut tumours displayed less CNAs. Gains were detected for
chromosomes 17q and 19p (57%). Most frequent losses affected
chromosomes 18 (43%) and 9p (21%).
CONCLUSIONSThe
results of our CGH analyses revealed new distinct candidate regions in
the human genome associated with sporadic neuroendocrine tumours. Some
of the genetic alterations were shared by foregut and midgut tumours
while others discriminated between the two groups. Thus our results
allude to the involvement of identical as well as discriminative
genetic loci in tumorigenesis and progression of neuroendocrine
neoplasms of the foregut and midgut. Based on these findings potential
new candidate genes will be discussed.
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