C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil
Autor(a) principal: | |
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Data de Publicação: | 2006 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://ar.iiarjournals.org/content/26/4B/2909.abstract http://repositorio.unifesp.br/handle/11600/42593 |
Resumo: | Background: The genetic events involved in gastric cancer, the third most frequent cancer in the world with a high incidence in Para State, Brazil, remain largely unknown. Materials and Methods: Twenty-one primary gastric adenocarcinomas were investigated by comparative genomic hybridization (CGH) and the relationships between genomic abnormalities and histopathological features were evaluated. Results: Eighty-one percent of cases presented DNA copy-number changes. Chromosomal gains were the most frequent finding, losses occurring only in the diffuse type. The main copy-number gains were on chromosome 8, principally on 8q24.1 (8121 cases), 8p21 (3121) and 8p23.28p12 (2121). Gain of region 8q24.1, where C-WC is located, was the main finding, exclusively in the intestinal type with metastasis. Conclusion: C-MYC locus amplification may be predictor of aggressiveness in intestinal-type gastric cancer, playing an important role in its development and progression. Moreover, other genes on 8q24 should be investigated. Gastric adenocarcinomas of differing histopathological features were associated with distinct genetic alterations, supporting the hypothesis that they evolve through distinct genetic pathways. |
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C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazilgastric cancercomparative genomic hybridization8q24Background: The genetic events involved in gastric cancer, the third most frequent cancer in the world with a high incidence in Para State, Brazil, remain largely unknown. Materials and Methods: Twenty-one primary gastric adenocarcinomas were investigated by comparative genomic hybridization (CGH) and the relationships between genomic abnormalities and histopathological features were evaluated. Results: Eighty-one percent of cases presented DNA copy-number changes. Chromosomal gains were the most frequent finding, losses occurring only in the diffuse type. The main copy-number gains were on chromosome 8, principally on 8q24.1 (8121 cases), 8p21 (3121) and 8p23.28p12 (2121). Gain of region 8q24.1, where C-WC is located, was the main finding, exclusively in the intestinal type with metastasis. Conclusion: C-MYC locus amplification may be predictor of aggressiveness in intestinal-type gastric cancer, playing an important role in its development and progression. Moreover, other genes on 8q24 should be investigated. Gastric adenocarcinomas of differing histopathological features were associated with distinct genetic alterations, supporting the hypothesis that they evolve through distinct genetic pathways.Univ Fed Para, Lab Citogenet Humana & Genet Toxicol, Dept Biol, Ctr Ciencias Biol, BR-66075900 Belem, Para, BrazilUniv Fed Sao Paulo, Div Genet, Dept Morphol, Sao Paulo, BrazilUniv Fed Para, Joao Barros Barreto Univ Hosp, Dept Pathol, Belem, Para, BrazilUniv Fed Para, Joao Barros Barreto Univ Hosp, Surg Serv 4, Belem, Para, BrazilUniv Fed Sao Paulo, Div Genet, Dept Morphol, Sao Paulo, BrazilWeb of ScienceInt Inst Anticancer ResearchUniv Fed ParaUniversidade Federal de São Paulo (UNIFESP)Burbano, Rommel Rodríguez [UNIFESP]Assumpcao, Paulo Pimentel de [UNIFESP]Leal, Mariana Ferreira [UNIFESP]Calcagno, Danielle Queiroz [UNIFESP]Guimaraes, Adriana CostaKhayat, Andre SalimTakeno, Sylvia Satomi [UNIFESP]Chen, Elizabeth Suchi [UNIFESP]Smith, Marilia de Arruda Cardoso [UNIFESP]2018-06-15T13:50:14Z2018-06-15T13:50:14Z2006-07-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion2909-2914http://ar.iiarjournals.org/content/26/4B/2909.abstractAnticancer Research. Athens: Int Inst Anticancer Research, v. 26, n. 4B, p. 2909-2914, 2006.0250-7005http://repositorio.unifesp.br/handle/11600/42593WOS:000241391600018engAnticancer Researchinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-05-02T13:59:23Zoai:repositorio.unifesp.br/:11600/42593Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-05-02T13:59:23Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
title |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
spellingShingle |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil Burbano, Rommel Rodríguez [UNIFESP] gastric cancer comparative genomic hybridization 8q24 |
title_short |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
title_full |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
title_fullStr |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
title_full_unstemmed |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
title_sort |
C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil |
author |
Burbano, Rommel Rodríguez [UNIFESP] |
author_facet |
Burbano, Rommel Rodríguez [UNIFESP] Assumpcao, Paulo Pimentel de [UNIFESP] Leal, Mariana Ferreira [UNIFESP] Calcagno, Danielle Queiroz [UNIFESP] Guimaraes, Adriana Costa Khayat, Andre Salim Takeno, Sylvia Satomi [UNIFESP] Chen, Elizabeth Suchi [UNIFESP] Smith, Marilia de Arruda Cardoso [UNIFESP] |
author_role |
author |
author2 |
Assumpcao, Paulo Pimentel de [UNIFESP] Leal, Mariana Ferreira [UNIFESP] Calcagno, Danielle Queiroz [UNIFESP] Guimaraes, Adriana Costa Khayat, Andre Salim Takeno, Sylvia Satomi [UNIFESP] Chen, Elizabeth Suchi [UNIFESP] Smith, Marilia de Arruda Cardoso [UNIFESP] |
author2_role |
author author author author author author author author |
dc.contributor.none.fl_str_mv |
Univ Fed Para Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Burbano, Rommel Rodríguez [UNIFESP] Assumpcao, Paulo Pimentel de [UNIFESP] Leal, Mariana Ferreira [UNIFESP] Calcagno, Danielle Queiroz [UNIFESP] Guimaraes, Adriana Costa Khayat, Andre Salim Takeno, Sylvia Satomi [UNIFESP] Chen, Elizabeth Suchi [UNIFESP] Smith, Marilia de Arruda Cardoso [UNIFESP] |
dc.subject.por.fl_str_mv |
gastric cancer comparative genomic hybridization 8q24 |
topic |
gastric cancer comparative genomic hybridization 8q24 |
description |
Background: The genetic events involved in gastric cancer, the third most frequent cancer in the world with a high incidence in Para State, Brazil, remain largely unknown. Materials and Methods: Twenty-one primary gastric adenocarcinomas were investigated by comparative genomic hybridization (CGH) and the relationships between genomic abnormalities and histopathological features were evaluated. Results: Eighty-one percent of cases presented DNA copy-number changes. Chromosomal gains were the most frequent finding, losses occurring only in the diffuse type. The main copy-number gains were on chromosome 8, principally on 8q24.1 (8121 cases), 8p21 (3121) and 8p23.28p12 (2121). Gain of region 8q24.1, where C-WC is located, was the main finding, exclusively in the intestinal type with metastasis. Conclusion: C-MYC locus amplification may be predictor of aggressiveness in intestinal-type gastric cancer, playing an important role in its development and progression. Moreover, other genes on 8q24 should be investigated. Gastric adenocarcinomas of differing histopathological features were associated with distinct genetic alterations, supporting the hypothesis that they evolve through distinct genetic pathways. |
publishDate |
2006 |
dc.date.none.fl_str_mv |
2006-07-01 2018-06-15T13:50:14Z 2018-06-15T13:50:14Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://ar.iiarjournals.org/content/26/4B/2909.abstract Anticancer Research. Athens: Int Inst Anticancer Research, v. 26, n. 4B, p. 2909-2914, 2006. 0250-7005 http://repositorio.unifesp.br/handle/11600/42593 WOS:000241391600018 |
url |
http://ar.iiarjournals.org/content/26/4B/2909.abstract http://repositorio.unifesp.br/handle/11600/42593 |
identifier_str_mv |
Anticancer Research. Athens: Int Inst Anticancer Research, v. 26, n. 4B, p. 2909-2914, 2006. 0250-7005 WOS:000241391600018 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Anticancer Research |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
2909-2914 |
dc.publisher.none.fl_str_mv |
Int Inst Anticancer Research |
publisher.none.fl_str_mv |
Int Inst Anticancer Research |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
_version_ |
1814268326561447936 |