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284篇 您的检索式:作者名="Calcagno"
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1Promoter hypermethylation of CDH1, FHIT, MTAP and PLAGL1 in gastric adenocarcinoma in individuals from Northern Brazil显示文摘AIM: To evaluate the methylation status of CDH1, FHIT, MTAP and PLAGL1 promoters and the association of these findings with clinico-pathological characteristics. METHODS: Methylation-specific PCR (MSP) assay was performed in 13 nonneoplastic gastric adenocarcinoma, 30 intestinal-type gastric adenocarcinoma and 35 diffuse- type gastric adenocarcinoma samples from individuals in Northern Brazil. Statistical analyses were performed using the chi-square or Fisher’s exact test to assess associations between methylation status and clinico- pathological characteristics. RESULTS: Hypermethylation frequencies of CDH1, FHIT, MTAP and PLAGL1 promoter were 98.7%, 53.9%, 23.1% and 29.5%, respectively. Hypermethylation of three or four genes revealed a significant association with diffuse-type gastric cancer compared with nonneoplastic cancer. A higher hypermethylation frequency wassignificantly associated with H pylori infection in gastric cancers, especially with diffuse-type. Cancer samples without lymph node metastasis showed a higher FHIT hypermethylation frequency. MTAP hypermethylation was associated with H pylori in gastric cancer samples, as well as with diffuse-type compared with intestinal-type. In diffuse-type, MTAP hypermethylation was associated with female gender. CONCLUSION: Our findings show differential gene methylation in tumoral tissue, which allows us to conclude that hypermethylation is associated with gastric carcinogenesis. MTAP promoter hypermethylation can be characterized as a marker of diffuse-type gastric cancer, especially in women and may help in diagnosis, prognosis and therapies. The H pylori infectious agent was present in 44.9% of the samples. This infection may be correlated with the carcinogenic process through the gene promoter hypermethylation, especially the MTAP promoter in diffuse-type. A higher H pylori infection in diffuse-type may be due to greater genetic predisposition.Mariana Ferreira Leal Eleonidas Moura Lima Patrícia Natália Oliveira Silva Paulo Pimentel Assumpo Danielle Queiroz Calcagno Spencer Luiz Marques Payo Rommel Rodríguez Burbano Marília de Arruda Cardoso Smith 2007World Journal of Gastroenterology2007,13,18:24
2DNA and histone methylation in gastric carcinogenesis显示文摘Epigenetic alterations contribute significantly to the development and progression of gastric cancer,one of the leading causes of cancer death worldwide.Epigenetics refers to the number of modifications of the chromatin structure that affect gene expression without altering the primary sequence of DNA,and these changes lead to transcriptional activation or silencing of the gene.Over the years,the study of epigenetic processes has increased,and novel therapeutic approaches that target DNA methylation and histone modifications have emerged.A greater understanding of epigenetics and the therapeutic potential of manipulating these processes is necessary for gastric cancer treatment.Here,we review recent research on the effects of aberrant DNA and histone methylation on the onset and progression of gastric tumors and the development of compounds that target enzymes that regulate the epigenome.Danielle Queiroz Calcagno Carolina Oliveira Gigek Elizabeth Suchi Chen Rommel Rodriguez Burbano Marília de Arruda Cardoso Smith 2013World Journal of Gastroenterology2013,19,8:14
3Role of mi RNAs and their potential to be useful as diagnostic and prognostic biomarkers in gastric cancer显示文摘Alterations in epigenetic control of gene expression play an important role in many diseases, including gastric cancer. Many studies have identified a large number of upregulated oncogenic mi RNAs and downregulated tumour-suppressor mi RNAs in this type of cancer. In this review, we provide an overview of the role of mi RNAs, pointing to their potential to be useful as diagnostic and/or prognostic biomarkers in gastric cancer. Moreover, we discuss the influence of polymorphisms and epigenetic modifications on mi RNA activity.Kelly Cristina da Silva Oliveira Taíssa Maíra Thomaz Araújo Camila Inagaki Albuquerque Gabriela Alcantara Barata Carolina Oliveira Gigek Mariana Ferreira Leal Fernanda Wisnieski Fernando Augusto Rodrigues Mello Junior André Salim Khayat Paulo Pimentel de Assumpcao Rommel Mário Rodriguez Burbano Marília Cardoso Smith Danielle Queiroz Calcagno 2016World Journal of Gastroenterology2016,22,35:11
4Interrelationship between chromosome 8 aneuploidy,C-MYC amplification and increased expression in individuals from northern Brazil with gastric adenocarcinoma显示文摘AIM: To investigate chromosome 8 numerical aberra- tions, C-MYC oncogene alterations and its expression in gastric cancer and to correlate these findings with histo- pathological characteristics of gastric tumors. METHODS: Specimens were collected surgically from seven patients with gastric adenocarcinomas. Immu- nostaining for C-MYC and dual-color fluorescence in situ hybridization (FISH) for C-MYC gene and chromosome 8 centromere were performed. RESULTS: All the cases showed chromosome 8 aneu- ploidy and C-MYC amplification, in both the diffuse and intestinal histopathological types of Lauren. No significant difference (P < 0.05) was observed between the level ofchromosome 8 ploidy and the site, stage or histological type of the adenocarcinomas. C-MYC high amplification, like homogeneously stained regions (HSRs) and double minutes (DMs), was observed only in the intestinal-type. Structural rearrangement of C-MYC, like translocation, was observed only in the diffuse type. Regarding C-MYC gene, a significant difference (P < 0.05) was observed between the two histological types. The C-MYC protein was expressed in all the studied cases. In the intestinal- type the C-MYC immunoreactivity was localized only in the nucleus and in the diffuse type in the nucleus and cytoplasm. CONCLUSION: Distinct patterns of alterations between intestinal and diffuse types of gastric tumors support the hypothesis that these types follow different genetic path- ways.Danielle Queiroz Calcagno Mariana Ferreira Leal Aline Damaceno Seabra Andre Salim Khayat Elizabeth Suchi Chen Samia Demachki Paulo Pimentel Assumpcao Mario Henrique Girao Faria Silvia Helena Barem Rabenhorst Márcia Valéria Pitombeira Ferreira Marília de Arruda Cardoso Smith Rommel Rodríguez Burbano 2006World Journal of Gastroenterology2006,12,38:9
5MYC and gastric adenocarcinoma carcinogenesis显示文摘MYC is an oncogene involved in cell cycle regulation,cell growth arrest,cell adhesion,metabolism,ribosome biogenesis,protein synthesis,and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer. In the present review,we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma carcinogenesis,including its association with Helicobacter pylori (H pylori) and clinical applications.Danielle Queiroz Calcagno Mariana Ferreira Leal Paulo Pimentel Assumpo Marília de Arruda Cardoso Smith Rommel Rodríguez Burbano 2008World Journal of Gastroenterology2008,14,39:8
6Clinical implication of 14-3-3 epsilon expression in gastric cancer显示文摘AIM:To evaluate for the first time the protein and mRNA expression of 14-3-3εin gastric carcinogenesis.METHODS:14-3-3εprotein expression was determined by western blotting,and mRNA expression was examined by real-time quantitative RT-PCR in gastric tumors and their matched non-neoplastic gastric tissue samples.RESULTS:Authors observed a significant reduction of 14-3-3εprotein expression in gastric cancer(GC)samples compared to their matched non-neoplastic tissue.Reduced levels of 14-3-3εwere also associated with diffuse-type GC and early-onset of this pathology.Our data suggest that reduced 14-3-3εmay have a role in gastric carcinogenesis process.CONCLUSION:Our results reveal that the reduced 14-3-3εexpression in GC and investigation of 14-3-3ε interaction partners may help to elucidate the carcino-genesis process.Mariana Ferreira Leal Danielle Queiroz Calcagno Smia Demachki Paulo Pimentel Assumpo Roger Chammas Rommel Rodríguez Burbano Marília de Arruda Cardoso Smith 2012World Journal of Gastroenterology2012,18,13:6
7Increased arterial stiffness in inflammatory bowel diseases is dependent upon inflammation and reduced by immunomodulatory drugs显示文摘Luca Zanoli Stefania Rastelli Gaetano Inserra Paolo Lentini Enrico Valvo Emanuela Calcagno Pierre Boutouyrie Stephane Laurent Pietro Castellino 2014Atherosclerosis2014,,2:2
8Nonalcoholic fatty liver disease and hepatocellular carcinoma: A weighty connection显示文摘Brad Q. Starley Christopher J. Calcagno Stephen A. Harrison 2010Hepatology2010,,5:2
9Regression of Inflammation in Atherosclerosis by the LXR Agonist R211945显示文摘Esad Vucic Claudia Calcagno Stephen D. Dickson James H.F. Rudd Katsumi Hayashi Jan Bucerius Erin Moshier Jessica S. Mounessa Michelle Roytman Matthew J. Moon James Lin Sarayu Ramachandran Tatsuo Tanimoto Karen Brown Masakatsu Kotsuma Sotirios Tsimikas Edw 2012JACC: Cardiovascular Imaging2012,,8:2
10Hydrogen effect on atomic configuration of keV-ion-irradiated carbon显示文摘Compagnini G Calcagno L Foti G 1992Phys Rev Lett1992,69,3:2
11Vascular endothelial growth factor stimulates organ2specific host mat rix metalloproteinase-9 expression and ovarian cancer invasion显示文摘Belotti D Calcagno C Garofalo A 2008Mol Cancer Res2008,6,4:1
12DCE-MRI of the liv- er: effect of linear and nonlinear conversions on hepatic perfusion quantification and reproducibility显示文摘Aronhime S Calcagno C Jajamovieh GH 2014J Magn Reson Imaging2014,40,:1
13Purification, cDNA cloning, and developmental changes in the steady-state mRNA level of rat testicular tissue inhibitor of metalloproteases-2 (TIMP-2) 显示文摘GRIMA J CALCAGNO K CHENG C Y 1996J Androl1996,17,3:1
14Imaging the Efficacy of Anti-Inflammatory Liposomes in a Rabbit Model of Atherosclerosis by Non-Invasive Imaging显示文摘Mark E. Lobatto Claudia Calcagno Josbert M. Metselaar Gert Storm Erik S.G. Stroes Zahi A. Fayad Willem J.M. Mulder 2012Methods in Enzymology2012,,:1
15Association of coffee and caffdne consumption with fatty liver disease, nonalcoholic steato- hepatitis, and degree of hepatic fibrosis显示文摘Molloy JW Calcagno CJ Williams CD 2012Hepamlogy2012,,55:1
16Clinical response to Thalidomide and colchicine in two siblings with Behcet’s disease carrying a single mutated MEFV allele显示文摘Rigante D La Torre F Calcagno G A 2012Rheumatol Int2012,32,6:1
17Compari-son of drug transporter levels in normal colon,colon cancer,and Caco-2 cells:impact on drug disposition and discovery显示文摘CALCAGNO A M LUDWIG J A FOSTEL J M 2006Mol Pharm2006,3,1:1
18High plant diversity is needed to maintain ecosystem services显示文摘Isbell F Calcagno V Hector A 2011Nature2011,477,7363:1
19Can waist circumferenceidentify children with the metabolic syndrome[J]显示文摘Hirschler V Aranda C Calcagno Mde L 0,,08:1
20Effects of aripiprazole,olanzapine,and haloperidol in a model of cognitive deficit of schizophrenia in rats:relationship with glutamate release in the medial prefrontal cortex显示文摘Carli M Calcagno E Mainolfi P 0,,03:1
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