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	Provedor de dados Genet. Mol. Biol. (3) BJMBR (1) Autor Ayres,Flávio Monteiro (2) Cruz,Aparecido Divino da (2) Bastos,Celso da Cunha (1) Brasileiro-Filho,G. (1) Fuzikawa,A.K. (1) Glickman,Barry W. (1) Haddad,L.A. (1) Momotuk,Euza Guimarães (1) Pena,S.D.J. (1) Sajantila,Antti (1) Steele,Patricia (1) Vauhkonen,Hanna (1) da-Cunha-Melo,J.R. (1) Mais... Palavra-chave Microsatellite instability (4) Mutator phenotype (2) Colorectal cancers (1) Colorectal carcinoma (1) Complex microsatellite (1) DCC (1) Finnish and Somali populations (1) Gastrointestinal tumors (1) Hprt (1) Ionizing radiation (1) Loss of heterozygosity (1) Microsatellite (1) Mismatch repair (1) Myeloid leukemia (1) P53 (1) Polymerase chain reaction (1) TK6 cells (1) Mais... Tipo do documento Info:eu-repo/semantics/article (4) Ano 2006 (2) 2004 (1) 1997 (1) País Brazil (4) Idioma Inglês (4)		Ordenar por:  Relevância Autor Título Ano Registros recuperados: 4 Primeira ... 1 ... Última Utilization of microsatellites for the analysis of genomic alterations in colorectal cancers in Brazil BJMBR Fuzikawa,A.K.; Haddad,L.A.; da-Cunha-Melo,J.R.; Brasileiro-Filho,G.; Pena,S.D.J.. Two different pathogenetic mechanisms are proposed for colorectal cancers. One, the so-called "classic pathway", is the most common and depends on multiple additive mutational events (germline and/or somatic) in tumor suppressor genes and oncogenes, frequently involving chromosomal deletions in key genomic regions. Methodologically this pathway is recognizable by the phenomenon of loss of heterozygosity. On the other hand, the "mutator pathway" depends on early mutational loss of the mismatch repair system (germline and/or somatic) leading to accelerated accumulation of gene mutations in critical target genes and progression to malignancy. Methodologically this second pathway is recognizable by the phenomenon of microsatellite instability. The distinction... Tipo: Info:eu-repo/semantics/article Palavras-chave: Polymerase chain reaction; Colorectal carcinoma; Microsatellite; P53; DCC; Microsatellite instability. Ano: 1997 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000800001 Intrinsic structural variation of the complex microsatellite marker MYCL1 in Finnish and Somali populations and its relevance to gastrointestinal tumors Genet. Mol. Biol. Vauhkonen,Hanna; Sajantila,Antti. The structurally complex MYCL1 microsatellite marker is often used to determine microsatellite instability in colorectal cancers but the allelic variation of this marker has remained largely uncharacterized in both populations and in cancers. Our study describes the allelic distributions of MYCL1 in Finnish (n = 117) and Somali population samples (n = 61) of non-related individuals and compares this distribution with the instability pattern obtained from 61 gastrointestinal tumors. Tipo: Info:eu-repo/semantics/article Palavras-chave: Colorectal cancers; Complex microsatellite; Gastrointestinal tumors; Microsatellite instability; Finnish and Somali populations. Ano: 2006 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572006000400005 Detection of mutator phenotype in Brazilian patients with acute and chronic myeloid leukemia Genet. Mol. Biol. Ayres,Flávio Monteiro; Momotuk,Euza Guimarães; Bastos,Celso da Cunha; Cruz,Aparecido Divino da. The multisteps of tumorigenesis involve the classic chromosomal instability and the mutator phenotype pathways featured by a predisposition to acquire mutations in tumor suppressor genes and oncogenes. Expansion and contraction of microsatellite sequences due to a deficient mismatch repair system are a marker of the mutator phenotype. Controversial results regarding the extent of microsatellite instability (MSI) have been reported in the development and progression of myeloid malignancies. Here, we investigated MSI and loss of heterozygosity (LOH) frequencies at the microsatellite loci BAT-26, D7S486, D8S135, ANK1, IFNA, TP53 and bcr of 19 Brazilian patients with acute (AML) and chronic myeloid leukemia (CML). One AML patient and one CML patient were... Tipo: Info:eu-repo/semantics/article Palavras-chave: Loss of heterozygosity; Microsatellite instability; Mismatch repair; Mutator phenotype; Myeloid leukemia. Ano: 2004 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572004000400003 Low doses of gamma ionizing radiation increase hprt mutant frequencies of TK6 cells without triggering the mutator phenotype pathway Genet. Mol. Biol. Ayres,Flávio Monteiro; Cruz,Aparecido Divino da; Steele,Patricia; Glickman,Barry W.. The TK6 lymphoblastoid cell line is known to be mismatch repair (MMR) and p53 proficient. Deficiency in MMR results in a mutator phenotype characterized by microsatellite instability (MSI) and increased hprt mutant frequency (MF). Increased hprt MF is also a biomarker of effect for exposure to ionizing radiation. In order to test if a mutator phenotype could be induced by low doses of gamma ionizing radiation, an hprt cloning assay and a MSI investigation were performed after radiation exposure. The spontaneous MF was 1.6 x 10-6. The groups exposed to 0.2, 0.5 and 1.0 Gy had hprt MFs of 2.3, 3.3 and 2.2 x 10-6, respectively. The spontaneous MSI frequency per allele in non-selected cells was 5.4 x 10-3, as evidenced at the loci D11S35, nm23-H1, D8S135 and... Tipo: Info:eu-repo/semantics/article Palavras-chave: Mutator phenotype; Hprt; Microsatellite instability; TK6 cells; Ionizing radiation. Ano: 2006 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572006000300027 Registros recuperados: 4 Primeira ... 1 ... Última

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