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18篇 您的检索式:作者名="Menigatti"
    题名 作者 年代 出处 被引量
1Chronic exposure to cigarette smoke condensate in vitro induces epithelial to mesenchymal transition-like changes in human bronchial epithelial cells,BEAS-2B显示文摘Veljkovic E Jiricny J Menigatti M 0,,:1
2Defective DNA mismatch repair determines a characteristic transcriptional profile in proximal colon cancers 显示文摘Massimiliano di Pietro Jacob Sabates Bellver Mirco Menigatti 2005Gastroenterology2005,129,3:1
3Preinvasive colorectal lesion transcriptomes correlate with endoscopic morphology (polypoid vs. nonpolypoid)显示文摘Elisa Cattaneo Endre Laczko Federico Buffoli Fausto Zorzi Maria Antonia Bianco Mirco Menigatti Zdena Bartosova Ritva Haider Birgit Helmchen Jacob Sabates‐Bellver Amit Tiwari Josef Jiricny Giancarlo Marra 2011EMBO Mol Med2011,,6:1
4Microsatellite instability and mismatch-repair protein expression in hereditary and sporadic colorectal carcinogenesis 显示文摘Borhgi F Menigatti M Benatti P 2001Cancer Res2001,61,3:1
5A compre- hensive look at transcription factor gene expression changes in col- orectal adenomas显示文摘Vonlanthen J Okoniewski MJ Menigatti M 2014BMC cancer2014,14,:1
6Normal colorectal mucosa exhibits sex-and segment-specific susceptibility to DNA methylation at the hMLH1 and MGMT prornoters显示文摘MENIGATTI M TRUNINGER K GEBBERS J O 2009Oneogene2009,28,6:1
7Microsatellite instability and mismatch repair protein expression and sporadic colorectal carcinogenesis显示文摘Borghi F Menigatti M Benatti P 2001Cancer Res2001,61,3:1
8A comprehensive look at transcxiption faclor gene expression changes in coloreclal adenomas 显示文摘Vonlanthen J Okoniewski M J Menigatti M 2014BMC Cancer2014,14,:1
9The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human colorectal tumorigenesis 显示文摘Menigatti M Cattaneo E Sabates-Bellver J 2009Mol Cancer2009,8,:1
10Pinl interacts with C-myb in a phosphorylation-dependent manner and regu- lates its transactivation activity显示文摘Pani E Menigatti M Schubert S 2008Biochim Biophys Acta2008,1783,6:1
11Chronic exposure to cigarette smoke condensate in vitro induces epithelial to mesenchymal transition-like changes in human bronchial epithelial cells, BEAS-2B显示文摘Veljkovic E Jiricny J Menigatti M 2011Toxicol In Vitro2011,25,2:1
12Methylation pattern of different regions of the MLH1 promoter and silencing of gene expression in hereditary and sporadic colorectal cancer显示文摘Menigatti M Di Gregorio C Borghi F 2001Genes Chromosomes Cancer2001,31,4:1
13Defective DNA mismatch repair determines a characteristic transcriptional profile in proximal colon cancers 显示文摘di Pietro M Sabates Bellver J Menigatti M 2005Gastroenterology2005,129,3:1
14Normal colorectal mucosa exhibits sex- and segment-specific susceptibility to DNA methylation at the hMLH1 and MGMT promoters 显示文摘Menigatti M Truninger K Gebbers JO 2009Oncogene2009,28,6:1
15A comprehen-sive look at transcription factor gene expression changes in color-eetal adenomas显示文摘Vonlanthen J Okoniewski MJ Menigatti M 2014BMC Cancer2014,14,:1
16Methylation pattern of different regions of the MLH1 promoter and silencing of gene ex pression in hereditary and sporadic colorectal cancer显示文摘Menigatti M Di Gregorio C Borghi F 2001Genes Chromosomes Cancer2001,31,4:1
17Epigenetic silencing of monoallelically methylated miRNA loci in precancerous colorectal lesions显示文摘Menigatti M Staiano T Manser CN 2013Oncogenesis2013,2,:1
18缺损DNA错配修复决定一个近侧结肠癌特异的转录模式显示文摘Background & Aims: Colon cancers with defective DNA mismatch repair (MMR) have peculiar molecular, pathologic, and clinical features, including high-level microsatellite instability, conspicuous lymphocytic infiltration, preferential location in the proximal colon, and better prognosis. Our aim was to characterize the transcriptional profile of this colon cancer subset. Methods: An oligonucleotide microarray containing 12,625 probes was used to evaluate gene expression in 25 proximal colon cancers, 10 samples of normal colon mucosa, and 14 colon cancer cell lines. Transcriptional profiles of MMR-deficient cancers and cell lines were compared with those of their MMR-proficient counterparts. Results: Unsupervised anal-ysis of microarray data showed that MMR status exerts a predominant influence on the gene expression profile of proximal colon cancers. Hierarchical clustering divided the cancers into 2 groups corresponding almost perfectly with their MMR status. Supervised analysis identified numerous gene expression changes that represent a genetic signature of MMR-deficient colon cancers. Changes in genes involved in apoptosis and the immune response were consistent with the better prognosis of MMR-deficient cancers. In MMR-deficient cancers and cell lines, 4-1BBL, a crucial gene in the anti-tumor immune response, was, respectively, 2.4 and 6.0 times more expressed than in their MMR-proficient counterparts. This difference was con- firmed by quantitative reverse-transcription polymerase chain reaction and flow cytometric assessment of 4-1BBL protein expression in colon cancer cell lines. Our analysis also showed novel possible gene targets of microsatellite instability. Conclusions: MMR inactivation produces distinct changes in the cellular messenger RNA pool, which is consistent with a unique tumorigenesis pathway.Di Pietro M. Bellver J.S. Menigatti M. G. Marra 陈云茹 2006世界核心医学期刊文摘(胃肠病学分册)2006,0,2:0
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