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DNA copy number profiles of gastric cancer precursor lesions
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...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2147033/ https://www.ncbi.nlm.nih.gov/pubmed/17908304 http://dx.doi.org/10.1186/1471-2164-8-345 |
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author | Buffart, Tineke E Carvalho, Beatriz Mons, Thomas Reis, Rui M Moutinho, Cátia Silva, Paula van Grieken, Nicole CT Vieth, Michael Stolte, Manfred van de Velde, Cornelis JH Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A |
author_facet | Buffart, Tineke E Carvalho, Beatriz Mons, Thomas Reis, Rui M Moutinho, Cátia Silva, Paula van Grieken, Nicole CT Vieth, Michael Stolte, Manfred van de Velde, Cornelis JH Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A |
author_sort | Buffart, Tineke E |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2147033 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-21470332007-12-19 DNA copy number profiles of gastric cancer precursor lesions Buffart, Tineke E Carvalho, Beatriz Mons, Thomas Reis, Rui M Moutinho, Cátia Silva, Paula van Grieken, Nicole CT Vieth, Michael Stolte, Manfred van de Velde, Cornelis JH Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A BMC Genomics Research Article 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. BioMed Central 2007-10-01 /pmc/articles/PMC2147033/ /pubmed/17908304 http://dx.doi.org/10.1186/1471-2164-8-345 Text en Copyright © 2007 Buffart et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Buffart, Tineke E Carvalho, Beatriz Mons, Thomas Reis, Rui M Moutinho, Cátia Silva, Paula van Grieken, Nicole CT Vieth, Michael Stolte, Manfred van de Velde, Cornelis JH Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A DNA copy number profiles of gastric cancer precursor lesions |
title | DNA copy number profiles of gastric cancer precursor lesions |
title_full | DNA copy number profiles of gastric cancer precursor lesions |
title_fullStr | DNA copy number profiles of gastric cancer precursor lesions |
title_full_unstemmed | DNA copy number profiles of gastric cancer precursor lesions |
title_short | DNA copy number profiles of gastric cancer precursor lesions |
title_sort | dna copy number profiles of gastric cancer precursor lesions |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2147033/ https://www.ncbi.nlm.nih.gov/pubmed/17908304 http://dx.doi.org/10.1186/1471-2164-8-345 |
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