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| 1 | Promoter 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 Assumpo Danielle Queiroz Calcagno Spencer Luiz Marques Payo Rommel Rodríguez Burbano Marília de Arruda Cardoso Smith | 2007 | World Journal of Gastroenterology2007，13，18： | 24 |
| 2 | DNA 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 | 2013 | World Journal of Gastroenterology2013，19，8： | 14 |
| 3 | Role 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 | 2016 | World Journal of Gastroenterology2016，22，35： | 11 |
| 4 | Interrelationship 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 | 2006 | World Journal of Gastroenterology2006，12，38： | 9 |
| 5 | MYC 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 Assumpo Marília de Arruda Cardoso Smith Rommel Rodríguez Burbano | 2008 | World Journal of Gastroenterology2008，14，39： | 8 |
| 6 | hsa-miR-29c and hsa-miR-135b differential expression aspotential biomarker of gastric carcinogenesis显示文摘AIM: To investigate the expression profiles of hsa-mi R-29 c and hsa-mi R-135 b in gastric mucosal samples and their values as gastric carcinogenesis biomarkers. METHODS: The expression levels of hsa-mi R-29 c and hsa-mi R-135 b in normal gastric mucosa, non-atrophic chronic gastritis, intestinal metaplasia and intestinaltype gastric adenocarcinoma were analysed using quantitative real-time PCR. The difference between hsa-mi R-29 c and hsa-mi R-135 b expression profiles in the grouped samples was evaluated by ANOVA and Student's t-test tests. The results were adjusted for multiple testing by using Bonferroni's correction. P values ≤ 0.05 were considered statistically significant. To evaluate hsa-mi R-29 c and hsa-mi R-135 b expressions as potential biomarkers of gastric carcinogenesis, we performed a receiver operating characteristic curve analysis and the derived area under the curve, and a Categorical Principal Components Analysis. In silico identification of the genetic targets of hsa-mi R-29 c and hsa-mi R-135 b was performed using different prediction tools, in order to identify possible genes involved in gastric carcinogenesis.RESULTS: The expression levels of hsa-mi R-29 c were higher in normal gastric mucosal samples, and decreased progressively in non-atrophic chronic gastritis samples, intestinal metaplasia samples and intestinal-type gastric adenocarcinoma samples. The expression of hsa-mi R-29 c in the gastric lesions showed that non-atrophic gastritis have an intermediate profile to gastric normal mucosa and intestinal-type gastric adenocarcinoma, and that intestinal metaplasia samples presented an expression pattern similar to that in intestinal-type gastric adenocarcinoma. This micro RNA(mi RNA) has a good discriminatory accuracy between normal gastric samples and(1) intestinal-type gastric adenocarcinoma; and(2) intestinal metaplasia, and regulates the DMNT3 A oncogene. hsa-mi R-135 b is up-regulated in non-atrophic chronic gastritis and intestinal metaplasia samples and down-regulated in normal gastric mucosa and intestinal-type gastric adenocarcinoma samples. Non-atrophic chronic gastritis and intestinal metaplasia are significantly different from normal gastric mucosa samples. hsa-mi R-135 b expression presented a greater discriminatory accuracy between normal samples and gastric lesions. This mi RNA was associated with Helicobacter pylori presence in non-atrophic chronic gastritis samples and regulates the APC and KLF4 tumour suppressor genes.CONCLUSION: Our results provide evidence of epigenetic alterations in non-atrophic chronic gastritis and intestinal metaplasia and suggest that hsa-mi R-29 c and hsa-mi R-135 b are promising biomarkers of gastric carcinogenesis. | Amanda Ferreira Vidal Aline MP Cruz Leandro Magalhães Adenilson L Pereira Ana KM Anaissi Nélisson CF Alves Paulo JBS Albuquerque Rommel MR Burbano Samia Demachki Ândrea Ribeiro-dos-Santos | 2016 | World Journal of Gastroenterology2016，22，6： | 7 |
| 7 | Clinical 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 Smia Demachki Paulo Pimentel Assumpo Roger Chammas Rommel Rodríguez Burbano Marília de Arruda Cardoso Smith | 2012 | World Journal of Gastroenterology2012，18，13： | 6 |
| 8 | Association between Helicobacterpylori, Epstein-Barr virus, human papillomavirus and gastric adenocarcinomas显示文摘AIM To correlate Helicobacter pylori(H. pylori), Epstein-Barr virus(EBV) and human papillomavirus(HPV) with gastric cancer(GC) cases in Pará State, Brazil.METHODS Tissue samples were obtained from 302 gastric adenocarcinomas. A rapid urease test was used to detect the presence of H. pylori, and the presence of the cagA gene in the HP-positive samples was confirmed by PCR. An RNA in situ hybridization test designed to complement Eber1 RNA was used to detect the presence of EBV in the samples, and the L1 region of HPV was detected using nested PCR. Positive HPV samples were genotyped and analyzed for E6 and E7 viral gene expression. Infections were also correlated with the clinical and pathological characteristics of the patients.RESULTS The majority of the 302 samples analyzed were obtained from men(65%) aged 55 years or older(67%) and were classified as the intestinal subtype(55%). All three pathogens were found in the samples analyzed in the present study(H. pylori : 87%, EBV: 20%, HPV: 3%). Overall, 78% of the H. pylori-positive(H. pylori+) samples were cag A +(H. pylori-cag A+), and there was an association between the cytotoxic product of this gene and EBV. Coinfections of H. pylori-cagA+ and EBV were correlated with the most advanced tumor stages. Although only 20% of the tumors were positive for EBV, infection with this virus was associated with distant metastasis. Only the HPV 16 and 18 strains were found in the samples, although no expression of the E6 and E7 oncoproteins was detected. The fundus of the stomach was the region least affected by the pathogens.CONCLUSION HPV was not involved in gastric tumorigenesis. Prophylactic and therapeutic measures against H. pylori and EBV may prevent the development of GC, especially the more aggressive forms. | Carolina Rosal Teixeira de Souza Marcelli Carolini Alves Almeida Andre Salim Khayat Emerson Lucena da Silva Paulo Cardoso Soares Luiz Claudio Chaves Rommel Mario Rodriguez Burbano | 2018 | World Journal of Gastroenterology2018，24，43： | 6 |
| 9 | Interleukin-1 beta polymorphisms, Helicobacter pylori infection in individuals from Northern Brazil with gastric adenocarcinoma显示文摘 | GATTI L L BURBANO R R De ASSUMPCAO P P | 2004 | Clin Exp Med2004，4，2： | 1 |
| 10 | Oxidation kinetics and effect of pH on the degradation of MTBE with Fenton reagent显示文摘 | Burbano A A Dionysiou D D Suidan MT | 2005 | Water Res2005，39，1： | 1 |
| 11 | Determination of phytates and lower inositol phosphates in spanish legumes by HPLC显示文摘 | C Burbano M Muzquiz A Osagie | 1995 | Food Chemistry1995，，52： | 1 |
| 12 | Degra-dation of MTBE intermediates using Fenton’sreagent显示文摘 | Burbano A A Dionysiou D D Richardson T L et a1 | 2002 | Journal of Environmental Engineering ASCE2002，128，9： | 1 |
| 13 | Lupines as a potential source of raffinose family oligosaccharides: pre parative method for their isolation and purification显示文摘 | Muzctuiz M Burbano C Pedrosa M M | 1999 | In dustrial Crops and Products1999，19，： | 1 |
| 14 | Karyotypic and histopathologic findings in an accessory breast显示文摘 | Burbano RR Barbien Neto J Casartelli C | 1999 | An Acad Bras Cienc1999，71，3： | 1 |
| 15 | Oxidation kinetics and effect of pH on the degradation of MTBE with Fenton reagent显示文摘 | Burbano A A Dionysiou D D Suidan M T | 2005 | Water Research2005，39，1： | 1 |
| 16 | Discontinuation of prolonged infusions of dexmedetomidine in critically ill children with heart disease显示文摘 | BURBANO N H OTERO A V BERRY D E | | 0，，01： | 1 |
| 17 | l,aminar buruiug velocities and flame stability analysis of hydrogeu/air premixed flames at low pressure 显示文摘 | PAREJA J BURBANO H J AMELL A | 2011 | International Journal of Hydrogen Energy2011，36，10： | 1 |
| 18 | Effect of oxygen in a thin-film rotating disk photocatalytic reactor显示文摘 | DIONYSIOU D D BURBANO A A SUIDAN M T | 2002 | Environ Sci Technol2002，36，17： | 1 |
| 19 | Effect of oxidant-to-substrate ratios on the degradation of MTBE with Fenton reagent 显示文摘 | Burbano A A Dionysiou D D Suidan M T | 2008 | Water Research2008，42，12： | 1 |
| 20 | Interleukin-6 polymorphisms,helicobacter pylori infection in adult brazilian patients with chronic gastritis and gastric adenocarcinoma显示文摘 | Gatti LL Burbano RR Zambaldi-Tunes M | 2007 | Arch Med Res2007，5，38： | 1 |
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