DNA copy number profiles of gastric cancer precursor lesions
Autor(a) principal: | |
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Data de Publicação: | 2007 |
Outros Autores: | , , , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/1822/9159 |
Resumo: | 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 yloric 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. |
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DNA copy number profiles of gastric cancer precursor lesionsScience & TechnologyChromosomal 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 yloric 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.Fundação para a Ciência e a Tecnologia (FCT)grant POCTI/CBO/41179/2001Dutch Cancer Society, grant-KWF 2004–3051BioMed Central (BMC)Universidade do MinhoBuffart, TinekeCarvalho, BeatrizMons, ThomasReis, R. M.Moutinho, CátiaSilva, PaulaGrieken, Nicole C. T. vanVieth, MichaelStolte, ManfredVelde, Cornelis J. H. van deSchrock, EvelinMatthaei, AnjaYlstra, BaukeCarneiro, FátimaMeijer, Gerrit A.2007-10-012007-10-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/1822/9159eng"BMC Genomics". ISSN 1471-2164. 8 (Oct. 2007) 1-10.1471-216410.1186/1471-2164-8-34517908304http://www.biomedcentral.cominfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-07-21T12:31:04Zoai:repositorium.sdum.uminho.pt:1822/9159Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T19:26:18.887608Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
DNA copy number profiles of gastric cancer precursor lesions |
title |
DNA copy number profiles of gastric cancer precursor lesions |
spellingShingle |
DNA copy number profiles of gastric cancer precursor lesions Buffart, Tineke Science & Technology |
title_short |
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_sort |
DNA copy number profiles of gastric cancer precursor lesions |
author |
Buffart, Tineke |
author_facet |
Buffart, Tineke Carvalho, Beatriz Mons, Thomas Reis, R. M. Moutinho, Cátia Silva, Paula Grieken, Nicole C. T. van Vieth, Michael Stolte, Manfred Velde, Cornelis J. H. van de Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A. |
author_role |
author |
author2 |
Carvalho, Beatriz Mons, Thomas Reis, R. M. Moutinho, Cátia Silva, Paula Grieken, Nicole C. T. van Vieth, Michael Stolte, Manfred Velde, Cornelis J. H. van de Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A. |
author2_role |
author author author author author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade do Minho |
dc.contributor.author.fl_str_mv |
Buffart, Tineke Carvalho, Beatriz Mons, Thomas Reis, R. M. Moutinho, Cátia Silva, Paula Grieken, Nicole C. T. van Vieth, Michael Stolte, Manfred Velde, Cornelis J. H. van de Schrock, Evelin Matthaei, Anja Ylstra, Bauke Carneiro, Fátima Meijer, Gerrit A. |
dc.subject.por.fl_str_mv |
Science & Technology |
topic |
Science & Technology |
description |
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 yloric 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. |
publishDate |
2007 |
dc.date.none.fl_str_mv |
2007-10-01 2007-10-01T00:00:00Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/1822/9159 |
url |
http://hdl.handle.net/1822/9159 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
"BMC Genomics". ISSN 1471-2164. 8 (Oct. 2007) 1-10. 1471-2164 10.1186/1471-2164-8-345 17908304 http://www.biomedcentral.com |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
BioMed Central (BMC) |
publisher.none.fl_str_mv |
BioMed Central (BMC) |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
instname_str |
Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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