|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 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 | 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 |
| 7 | hTERT, MYC and TP53 deregulation in gastric preneoplastic lesions 显示文摘 | Tanielly Cristina Raiol Silva Mariana Ferreira Leal Danielle Quei- roz Calcagno | 2012 | BMC Gastroenterology2012，12，1： | 1 |
| 8 | hTERT methylation and expression in gastric cancer显示文摘 | Carolina Oliveira Gigek Mariana Ferreira Leal Patricia Natalia Oliveira Silva Luara Carolina Frias Lisboa Eleonidas Moura Lima Danielle Queiroz Calcagno Paulo Pimentel Assump??o Rommel Rodriguez Burbano Marilia de Arruda Cardoso Smith | 2009 | Biomarkers2009，，8： | 1 |
| 9 | Piwi like RNA-mediated gene silencing 1 gene as a possible major player in gastric cancer显示文摘AIM To establish a permanent piwi like RNA-mediated genesilencing 1(PIWIL1) gene knockout in AGP01 gastric cancer cell line using CRISPR-Cas9 system and analyze phenotypic modifications as well as gene expression alterations.METHODS CRISPR-Cas9 system used was purchased from Dharmacon GE Life Sciences(Lafayette, CO, United States) and permanent knockout was performed according to manufacturer's recommendations. Woundhealing assay was performed to investigate the effect of PIWIL1 knockout on migration capability of cells and Boyden chamber invasion assay was performed to investigate the effect on invasion capability. For the gene expression analysis, a one-color microarray-based gene expression analysis kit(Agilent Technologies, Santa Clara, CA, United States) was used according to the protocol provided by the manufacturer. RESULTS PIWIL1 gene knockout caused a significant decrease in AGP01 migration capacity as well as a significant decrease in cell invasiveness. Moreover, functional analysis based on grouping of all differentially expressed m RNAs identified a total of 35 genes(5 up-regulated and 30 down-regulated) encoding proteins involved in cellular invasion and migration. According to current literature, 9 of these 35 genes(DOCK2, ZNF503, PDE4 D, ABL1, ABL2, LPAR1, SMAD2, WASF3 and DACH1) are possibly related to the mechanisms used by PIWIL1 to promote carcinogenic effects related to migration and invasion, since their functions are consistent with the changes observed(being up-or down-regulated after knockout). CONCLUSION Taken together, these data reinforce the idea that PIWIL1 plays a crucial role in the signaling pathway of gastric cancer, regulating several genes involved in migration and invasion processes; therefore, its use as a therapeutic target may generate promising results in the treatment of gastric cancer. | Taíssa Araújo Andre Khayat Luciana Quintana Danielle Calcagno Ronald Mourao Antonio Modesto Juliana Paiva Adhara Lima Fabiano Moreira Edivaldo Oliveira Michel Souza Moneeb Othman Thomas Liehr Eliana Abdelhay Renata Gomes Sidney Santos Paulo Assumpcao | 2018 | World Journal of Gastroenterology2018，24，47： | 1 |
| 10 | Establishment and conventional cytogenetic characterization of three gastric cancer cell lines显示文摘 | Mariana Ferreira Leal José Luiz Martins do Nascimento Carla Elvira Araújo da Silva Maria Fernanda Vita Lamar?o Danielle Queiroz Calcagno André Salim Khayat Paulo Pimentel Assump??o Isabel Rosa Cabral Marília de Arruda Cardoso Smith Rommel Rodríguez Burban | 2009 | Cancer Genetics and Cytogenetics2009，，1： | 1 |
| 11 | Reference genes for quantitative RT-PCR data in gastric tissues and cell lines显示文摘AIM:To evaluate the suitability of reference genes in gastric tissue samples and cell lines.METHODS:The suitability of genes ACTB,B2M,GAPDH,RPL29,and 18S rRNA was assessed in21 matched pairs of neoplastic and adjacent nonneoplastic gastric tissues from patients with gastric adenocarcinoma,27 normal gastric tissues from patients without cancer,and 4 cell lines using reverse transcription quantitative real-time polymerase chain reaction(RT-qPCR).The ranking of the best single and combination of reference genes was determined by NormFinder,geNorm,BestKeeper,and DataAssist.In addition,GenEx software was used to determine the optimal number of reference genes.To validate the results,the mRNA expression of a target gene,DNMT1,was quantified using the different reference gene combinations suggested by the various software packages for normalization.RESULTS:ACTB was the best reference gene for all gastric tissues,cell lines and all gastric tissues plus cell lines.GAPDH+B2M or ACTB+B2M was the best combination of reference genes for all the gastric tissues.On the other hand,ACTB+B2M was the best combination for all the cell lines tested and was also the best combination for analyses involving all the gastric tissues plus cell lines.According to the GenEx software,2 or 3 genes were the optimal number of references genes for all the gastric tissues.The relative quantification of DNMT1 showed similar patterns when normalized by each combination of reference genes.The level of expression of DNMT1 in neoplastic,adjacent non-neoplastic and normal gastric tissues did not differ when these samples were normalized using GAPDH+B2M(P=0.32),ACTB+B2M(P=0.61),or GAPDH+B2M+ACTB(P=0.44).CONCLUSION:GAPDH+B2M or ACTB+B2M is the best combination of reference gene for all the gastric tissues,and ACTB+B2M is the best combination for the cell lines tested. | Fernanda Wisnieski Danielle Queiroz Calcagno Mariana Ferreira Leal Leonardo Caires dos Santos Carolina de Oliveira Gigek Elizabeth Suchi Chen Thaís Brilhante Pontes Paulo Pimentel Assumpo Mnica Barauna de Assumpo Smia Demachki Rommel Rodríguez Burbano Marília de Arruda Cardoso Smith | 2013 | World Journal of Gastroenterology2013，19，41： | 0 |
| 12 | Metastasis-associated lung adenocarcinoma transcript 1 molecular mechanisms in gastric cancer progression显示文摘Gastric cancer(GC)remains among the most common cancers worldwide with a high mortality-to-incidence ratio.Accumulated evidence suggests that long noncoding RNAs(lncRNAs)are involved in gastric carcinogenesis.These transcripts are longer than 200 nucleotides and modulate gene expression at multiple molecular levels,inducing or inhibiting biological processes and diseases.Metastasis-associated lung adenocarcinoma transcript 1(MALAT1)is one of the best-studied lncRNAs with comprehensive actions contributing to cancer progression.This lncRNA regulates gene expression at the transcriptional and posttranscriptional levels through interactions with microRNAs and proteins.In the present review,we discussed the molecular mechanism of MALAT1 and summarized the current knowledge of its expression in GC.Moreover,we highlighted the potential use of MALAT1 as a biomarker,including liquid biopsy. | Daniel Mateus de Oliveira Batista Jessica Manoelli Costa da Silva Carolina de Oliveira Gigek Marilia de Arruda Cardoso Smith Paulo Pimentel de Assumpcao Danielle Queiroz Calcagno | 2023 | World Journal of Gastrointestinal Oncology2023，15，9： | 0 |
| 13 | Identification of IL11RA and MELK amplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines显示文摘AIM To identify common copy number alterations on gastric cancer cell lines.METHODS Four gastric cancer cell lines(ACP02, ACP03, AGP01 and PG100) underwent chromosomal comparative genome hybridization and array comparative genome hybridization. We also confirmed the results by fluorescence in situ hybridization analysis using the bacterial artificial chromosome clone and quantitative real time PCR analysis.RESULTS The amplification of 9p13.3 was detected in all cell lines by both methodologies. An increase in the copy number of 9p13.3 was also confirmed by fluorescence in situ hybridization analysis. Moreover, the interleukin 11 receptor alpha(IL11RA) and maternal embryonic leucine zipper kinase(MELK) genes, which are present in the 9p13.3 amplicon, revealed gains of the MELK gene in all the cell lines studied. Additionally, a gain in the copy number of IL11 RA and MELK was observed in 19.1%(13/68) and 55.9%(38/68) of primary gastric adenocarcinoma samples, respectively. CONCLUSION The characterization of a small gain region at 9p13.3 in gastric cancer cell lines and primary gastric adenocarcinoma samples has revealed MELK as a candidate target gene that is possibly related to the development of gastric cancer. | Danielle Queiroz Calcagno Sylvia Santomi Takeno Carolina Oliveira Gigek Mariana Ferreira Leal Fernanda Wisnieski Elizabeth Suchi Chen Taíssa Maíra Thomaz Araújo Eleonidas Moura Lima Maria Isabel Melaragno Samia Demachki Paulo Pimentel Assumpcao Rommel Rodriguez Burbano Marília Cardoso Smith | 2016 | World Journal of Gastroenterology2016，22，43： | 0 |
| 14 | Traps and trumps from adjacent-to-tumor samples in gastric cancer research显示文摘The search for cancer biomarkers is frequently based on comparisons between tumors and adjacent-to-tumor samples. However, even after histological confirmation of been free of cancer cells, these adjacent-to-tumor samples might harbor molecular alterations which are not sufficient to cause them to look like cancer, but can differentiate these cells from normal cells. When comparing them, potential biomarkers are missed, and mainly the opportunity of finding initial aberrations presents in both tumors and adjacent samples, but not in true normal samples from non-cancer patients, resulting in misinterpretations about the carcinogenic process. Nevertheless,collecting adjacent-to-tumor samples brings trumps to be explored. The addition of samples from non-cancer patients opens an opportunity to increase the finds of the molecular cascade of events in the carcinogenic process.Differences between normal samples and adjacent samples might represent the first steps of the carcinogenic process. Adding samples of non-cancer patients to the analysis of molecular alterations relevant to the carcinogenic process opens a new window of opportunities to the discovery of cancer biomarkers and molecular targets. | Paulo Pimentel de Assumpcao Andre Salim Khayat Taissa Maira Thomaz Araujo Williams Fernandes Barra Geraldo Ishak Mine Maria Pereira Cruz Ramos Sidney Emanuel Batista dos Santos Andrea Kely Campos Ribeiro dos Santos Samia Demachki Paula Barauna de Assumpcao Danielle Queiroz Calcagno Ney Pereira Carneiro dos Santos Monica Barauna de Assumpcao Fabiano Cordeiro Moreira Andre Mauricio Ribeiro dos Santos Carolina Barauna de Assumpcao Gregory Joseph Riggins Rommel Mario Rodriguez Burbano | 2018 | Chinese Journal of Cancer Research2018，30，5： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员