Open Access Research article

DNA copy number profiles of gastric cancer precursor lesions

Tineke E Buffart1, Beatriz Carvalho12*, Thomas Mons1, Rui M Reis3, Cátia Moutinho2, Paula Silva2, Nicole CT van Grieken1, Michael Vieth4, Manfred Stolte4, Cornelis JH van de Velde5, Evelin Schrock6, Anja Matthaei6, Bauke Ylstra1, Fátima Carneiro27 and Gerrit A Meijer1

Author Affiliations

1 Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands

2 Institute of Pathology and Molecular Immunology of University of Porto – IPATIMUP, Porto, Portugal

3 Life and Health Sciences Research Institute (ICVS), Health Sciences School, University of Minho, Portugal

4 Institute of Pathology, Klinikum Bayreuth, Bayreuth, Germany

5 Dept. Surgery, Leiden University Medical Center, Leiden, The Netherlands

6 Institute of Clinical Genetics, University of Technology, Dresden, Dresden, Germany

7 Faculty of Medicine, University of Porto and Hospital, S. Joao, Porto, Portugal

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BMC Genomics 2007, 8:345  doi:10.1186/1471-2164-8-345

Published: 1 October 2007

Abstract

Background

Chromosomal instability (CIN) is the most prevalent type of genomic instability in gastric tumours, but its role in malignant transformation of the gastric mucosa is still obscure. In the present study, we set out to study whether two morphologically distinct categories of gastric cancer precursor lesions, i.e. intestinal-type and pyloric gland adenomas, would carry different patterns of DNA copy number changes, possibly reflecting distinct genetic pathways of gastric carcinogenesis in these two adenoma types.

Results

Using a 5K BAC array CGH platform, we showed that the most common aberrations shared by the 11 intestinal-type and 10 pyloric gland adenomas were gains of chromosomes 9 (29%), 11q (29%) and 20 (33%), and losses of chromosomes 13q (48%), 6(48%), 5(43%) and 10 (33%). The most frequent aberrations in intestinal-type gastric adenoma were gains on 11q, 9q and 8, and losses on chromosomes 5q, 6, 10 and 13, whereas in pyloric gland gastric adenomas these were gains on chromosome 20 and losses on 5q and 6. However, no significant differences were observed between the two adenoma types.

Conclusion

The results suggest that gains on chromosomes 8, 9q, 11q and 20, and losses on chromosomes 5q, 6, 10 and 13, likely represent early events in gastric carcinogenesis. The phenotypical entities, intestinal-type and pyloric gland adenomas, however, do not differ significantly (P = 0.8) at the level of DNA copy number changes.