Base de dados : MEDLINE
Pesquisa : G02.111.570.080.689.675 [Categoria DeCS]
Referências encontradas : 127181 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 12719 ir para página                         

  1 / 127181 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29408272
[Au] Autor:Saif I; Kasmi Y; Allali K; Ennaji MM
[Ad] Endereço:Team of Virology, Oncology and Medical Biotechnologies, Laboratory of Virology, Microbiology, Quality and Biotechnologies/ETB, Faculty of Science sand Technologies-Mohammedia, Hassan II University of Casablanca, Morocco.
[Ti] Título:Prediction of DNA methylation in the promoter of gene suppressor tumor.
[So] Source:Gene;651:166-173, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The epigenetics methylation of cytosine is the most common epigenetic form in DNA sequences. It is highly concentrated in the promoter regions of the genes, leading to an inactivation of tumor suppressors regardless of their initial function. In this work, we aim to identify the highly methylated regions; the cytosine-phosphate-guanine (CpG) island located on the promoters and/or the first exon gene known for their key roles in the cell cycle, hence the need to study gene-gene interactions. The Frommer and hidden Markov model algorithms are used as computational methods to identify CpG islands with specificity and sensitivity up to 76% and 80%, respectively. The results obtained show, on the one hand, that the genes studied are suspected of developing hypermethylation in the promoter region of the gene involved in the case of a cancer. We then showed that the relative richness in CG results from a high level of methylation. On the other hand, we observe that the gene-gene interaction exhibits co-expression between the chosen genes. This let us to conclude that the hidden Markov model algorithm predicts more specific and valuable information about the hypermethylation in gene as a preventive and diagnostics tools for the personalized medicine; as that the tumor-suppresser-genes have relative co-expression and complementary relations which the hypermethylation affect in the samples studied in our work.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
Ilhas de CpG
Metilação de DNA
Genes Supressores de Tumor
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Algoritmos
DNA de Neoplasias
Conjuntos de Dados como Assunto
Epistasia Genética
Seres Humanos
Cadeias de Markov
Modelos Genéticos
Neoplasias/genética
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  2 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29408271
[Au] Autor:Ben Khelifa S; Martinez R; Dandana A; Khochtali I; Ferchichi S; Castaño L
[Ad] Endereço:Unit of Clinical and Molecular Biology/UR17ES29, Faculty of Pharmacy, Monastir, Tunisia. Electronic address: souhaira34@gmail.com.
[Ti] Título:Maturity Onset Diabetes of the Young (MODY) in Tunisia: Low frequencies of GCK and HNF1A mutations.
[So] Source:Gene;651:44-48, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Maturity Onset Diabetes of the Young (MODY) is a monogenic form of diabetes characterized by autosomal dominant inheritance, an early clinical onset and a primary defect in ß-cell function. Mutations in the GCK and HNF1A genes are the most common cause of MODY among Caucasians. The etiology of MODY in Tunisia stills a challenge for researchers. The aim of this study was to screen for mutations in GCK, HNF1A, HNF4A and INS genes in North African Tunisians subjects, in whom the clinical profile was very suggestive of MODY. A total of 23 unrelated patients, with clinical presentation of MODY were tested for mutations in GCK, HNF1A, HNF4A and INS genes, using Denaturing High Performance Liquid Chromatography (DHPLC), Multiplex Ligation-depend Probe Amplification (MLPA) and sequencing analysis. We identified the previously reported mutation c-169C > T in one patient as well as a new mutation c-457C > T in two unrelated patients. No mutations were detected in the HNF1A and INS genes. Despite restrictive clinical criteria used for selecting patients in this study, the most common genes known for MODY do not explain the majority of cases in Tunisians. This suggests that there are others candidate or unidentified genes contributing to the etiology of MODY in Tunisians families.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/genética
Glucoquinase/genética
Fator 1-alfa Nuclear de Hepatócito/genética
Mutação
[Mh] Termos MeSH secundário: Adulto
Feminino
Frequência do Gene
Fator 4 Nuclear de Hepatócito/genética
Seres Humanos
Masculino
Polimorfismo Genético
Regiões Promotoras Genéticas
Proteínas Serina-Treonina Quinases
Tunísia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HNF1A protein, human); 0 (HNF4A protein, human); 0 (Hepatocyte Nuclear Factor 1-alpha); 0 (Hepatocyte Nuclear Factor 4); EC 2.7.1.2 (Glucokinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (germinal center kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  3 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29385191
[Au] Autor:Chuerduangphui J; Ekalaksananan T; Chaiyarit P; Patarapadungkit N; Chotiyano A; Kongyingyoes B; Promthet S; Pientong C
[Ad] Endereço:Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Effects of arecoline on proliferation of oral squamous cell carcinoma cells by dysregulating c-Myc and miR-22, directly targeting oncostatin M.
[So] Source:PLoS One;13(1):e0192009, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline, the major alkaloid of areca nut, is known to induce oral carcinogenesis, however, its mechanism is still needed to elucidate. This study investigated the effects of arecoline on cell viability and cell-cycle progression of oral squamous cell carcinoma (OSCC) cells as well as a relevant cellular gene expression. The results showed that a low concentration of arecoline (0.025 µg/ml) increased OSCC cell viability, proportion of cells in G2/M phase and cell proliferation. Simultaneously, it induced IL-6, STAT3 and c-Myc expression. Interestingly, c-myc promoter activity was also induced by arecoline. MiR-22 expression in arecoline-treated OSCC cells was suppressed and comparable to an upregulated c-Myc expression. In arecoline-treated OSCC cells, oncostatin M (OSM) expression was significantly upregulated and inversely correlated with miR-22 expression. Likewise, OSM expression and its post-transcriptional activity were significantly decreased in miR-22-transfected OSCC and 293FT cells. This result demonstrated that miR-22 directly targeted OSM. Interestingly, miR-22 played an important role as a tumor suppresser on suppressing cell proliferation, migration and cell-cycle progression of OSCC cells. This result suggested the effect of arecoline to promote cell proliferation and cell-cycle progression of OSCC cells might be involved in induction of c-Myc expression and reduction of miR-22 resulting in OSM upregulation.
[Mh] Termos MeSH primário: Arecolina/farmacologia
Carcinoma de Células Escamosas/patologia
Proliferação Celular/efeitos dos fármacos
MicroRNAs/metabolismo
Neoplasias Bucais/patologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Interleucina-6/biossíntese
MicroRNAs/genética
Neoplasias Bucais/metabolismo
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-myc/genética
Fator de Transcrição STAT3/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (MIRN22 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 4ALN5933BH (Arecoline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192009


  4 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29382572
[Au] Autor:Lv C; Mo C; Liu H; Wu C; Li Z; Li J; Wang Y
[Ad] Endereço:Key Laboratory of Bio-resources and Eco-environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, PR China.
[Ti] Título:Dopamine D2-like receptors (DRD2 and DRD4) in chickens: Tissue distribution, functional analysis, and their involvement in dopamine inhibition of pituitary prolactin expression.
[So] Source:Gene;651:33-43, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dopamine (DA) D2-like (and D1-like) receptors are suggested to mediate the dopamine actions in the anterior pituitary and/or CNS of birds. However, the information regarding the structure, functionality, and expression of avian D2-like receptors have not been fully characterized. In this study, we cloned two D2-like receptors (cDRD2, cDRD4) from chicken brain using RACE PCR. The cloned cDRD4 is a 378-amino acid receptor, which shows 57% amino acid (a.a.) identity with mouse DRD4. As in mammals, two cDRD2 isoforms, cDRD2L (long isoform, 437 a.a.) and cDRD2S (short isoform, 408 a.a.), which differ in their third intracellular loop, were identified in chickens. Using cell-based luciferase reporter assays or Western blot, we demonstrated that cDRD4, cDRD2L and cDRD2S could be activated by dopamine and quinpirole (a D2-like receptor agonist) dose-dependently, and their activation inhibits cAMP signaling pathway and stimulates MAPK/ERK signaling cascade, indicating that they are functional receptors capable of mediating dopamine actions. Quantitative real-time PCR revealed that cDRD2 and cDRD4 are widely expressed in chicken tissues with abundant expression noted in anterior pituitary, and their expressions are likely controlled by their promoters near exon 1, as demonstrated by dual-luciferase reporter assays in DF-1 cells. In accordance with cDRD2/cDRD4 expression in the pituitary, DA or quinpirole could partially inhibit vasoactive intestinal peptide-induced prolactin expression in cultured chick pituitary cells. Together, our data proves the functionality of DRD2 and DRD4 in birds and aids to uncover the conserved roles of DA/D2-like receptor system in vertebrates, such as its action on the pituitary.
[Mh] Termos MeSH primário: Galinhas/metabolismo
Dopamina/metabolismo
Hipófise/metabolismo
Prolactina/biossíntese
Receptores de Dopamina D2/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Galinhas/genética
Clonagem Molecular
DNA Complementar
Feminino
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Prolactina/antagonistas & inibidores
Regiões Promotoras Genéticas
Receptores de Dopamina D2/genética
Receptores de Dopamina D2/fisiologia
Transdução de Sinais
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Dopamine D2); 9002-62-4 (Prolactin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE


  5 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381741
[Au] Autor:Ettaki H; Troncoso-Ponce MA; To A; Barthole G; Lepiniec L; Baud S
[Ad] Endereço:Institut Jean-Pierre Bourgin, Institut National de la Recherche Agronomique, AgroParisTech, Centre National de la Recherche Scientifique, Université Paris-Saclay, Versailles, France.
[Ti] Título:Overexpression of MYB115, AAD2, or AAD3 in Arabidopsis thaliana seeds yields contrasting omega-7 contents.
[So] Source:PLoS One;13(1):e0192156, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Omega-7 monoenoic fatty acids (ω-7 FAs) are increasingly exploited both for their positive effects on health and for their industrial potential. Some plant species produce fruits or seeds with high amounts of ω-7 FAs. However, the low yields and poor agronomic properties of these plants preclude their commercial use. As an alternative, the metabolic engineering of oilseed crops for sustainable ω-7 FA production has been proposed. Two palmitoyl-ACP desaturases (PADs) catalyzing ω-7 FA biosynthesis were recently identified and characterized in Arabidopsis thaliana, together with MYB115 and MYB118, two transcription factors that positively control the expression of the corresponding PAD genes. In the present research, we examine the biotechnological potential of these new actors of ω-7 metabolism for the metabolic engineering of plant-based production of ω-7 FAs. We placed the PAD and MYB115 coding sequences under the control of a promoter strongly induced in seeds and evaluated these different constructs in A. thaliana. Seeds were obtained that exhibit ω-7 FA contents ranging from 10 to >50% of the total FAs, and these major compositional changes have no detrimental effect on seed germination.
[Mh] Termos MeSH primário: Arabidopsis/genética
Ácidos Graxos/metabolismo
Genes de Plantas
Sementes/genética
[Mh] Termos MeSH secundário: Arabidopsis/embriologia
Arabidopsis/metabolismo
Germinação
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Fatty Acids)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192156


  6 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29374520
[Au] Autor:Chen J; Jiang Y; Zhou J; Liu S; Qin N; Du J; Jin G; Hu Z; Ma H; Shen H; Dai J
[Ad] Endereço:Department of Epidemiology, School of Public Health, Nanjing Medical University, Nanjing, China; Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Medicine, Nanjing Medical University, Nanjing, China.
[Ti] Título:Evaluation of CpG-SNPs in miRNA promoters and risk of breast cancer.
[So] Source:Gene;651:1-8, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:CpG-SNPs in gene promoter regions are proposed to be associated with multiple diseases. To date, few studies have focused on the associations between CpG-SNPs in miRNA promoters and the risk of breast cancer. In this study, 138 miRNAs differentially expressed between breast cancer and non-cancer tissues (fold change >2, P < 0.05) were identified using The Cancer Genome Atlas (TCGA) Research database. In total, 13 SNPs were selected in the promoters of the miRNAs and were evaluated in a case-control study of Chinese women including 1486 cases and 1519 controls. After multivariate logistic regression analysis, we found that three CpG-SNPs: rs1190983, rs155247, and rs62382272, were significantly associated with breast-cancer susceptibility in the population (Additive model: rs1190983: adjusted OR = 0.88, 95% CI: 0.79-0.99, P = 0.034; rs155247: adjusted OR = 0.83, 95% CI: 0.74-0.93, P = 0.002; rs62382272: adjusted OR = 1.24, 95% CI: 1.04-1.47, P = 0.016). eQTL analysis showed that these three SNPs were correlated with the expression of the related miRNAs in TCGA breast cancer tissues (P = 0.006,0.009,0.001 for rs1190983, rs155247, and rs62382272). Furthermore, rs1190983 was found to be associated with CpG site (cg20488673) methylation (meQTL) (P = 0.004), which was in turn correlated with miR-342 expression (P = 0.016). These findings indicated that the three CpG-SNPs in the promoters of miRNAs were likely to possess important biological functions to breast cancer in the Han Chinese population.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Ilhas de CpG
MicroRNAs/genética
Polimorfismo de Nucleotídeo Único
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
Feminino
Predisposição Genética para Doença
Seres Humanos
Meia-Idade
Locos de Características Quantitativas
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  7 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29442031
[Au] Autor:Peng Y; Xu B; Tang J; Wan Z; Sun H; Wang G; Zhu YS
[Ti] Título:Analysis of ABCG2 methylation in stool samples of Chinese healthy males by pyrosequencing.
[So] Source:Pharmazie;71(8):447-454, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:ABCG2, an efflux pump protein-BCRP coding gene, is involved in the acquisition of chemotherapeutic drug resistance. In recent years, the epigenetic regulation of ABCG2, such as DNA methylation, has become a research hotspot and been attracting widespread attention. Methylation Special PCR (MSP) has been the mainly used method for gene methylation detection for a long time. With the development of pyrosequencing (PSQ) instrument and the convenience, simpleness, and economical benefit it brings, it will become the mainstream method for gene methylation detection in the near future. This study aims to establish a pyrosequencing method for detecting the methylation sites on ABCG2 gene promoter up-stream region, the promoter region and the first exon region, and to detect the methylation level of each site in stool samples, respectively. Thus, it cannot only lay the methodological foundation for the study of BCRP-mediated multi-drug resistance mechanisms in tumor cells, but also can give knowledge of ABCG2 methylation distribution in the intestine of Chinese healthy males by detecting the ABCG2 methylation levels in stool samples as the exfoliated intestinal epithelial cells constantly shed into the stool.
[Mh] Termos MeSH primário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética
Fezes/química
Proteínas de Neoplasias/genética
Análise de Sequência de Proteína/métodos
[Mh] Termos MeSH secundário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Adulto
Grupo com Ancestrais do Continente Asiático
Ilhas de CpG/genética
Metilação de DNA
Epigênese Genética
Éxons
Voluntários Saudáveis
Seres Humanos
Masculino
Proteínas de Neoplasias/metabolismo
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ABCG2 protein, human); 0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Neoplasm Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6559


  8 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29348663
[Au] Autor:Miao Y; Ajami NE; Huang TS; Lin FM; Lou CH; Wang YT; Li S; Kang J; Munkacsi H; Maurya MR; Gupta S; Chien S; Subramaniam S; Chen Z
[Ad] Endereço:Department of Diabetes Complications and Metabolism, Beckman Research Institute, City of Hope, 1500 Duarte Rd., Duarte, CA, 91010, USA.
[Ti] Título:Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function.
[So] Source:Nat Commun;9(1):292, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The optimal expression of endothelial nitric oxide synthase (eNOS), the hallmark of endothelial homeostasis, is vital to vascular function. Dynamically regulated by various stimuli, eNOS expression is modulated at transcriptional, post-transcriptional, and post-translational levels. However, epigenetic modulations of eNOS, particularly through long non-coding RNAs (lncRNAs) and chromatin remodeling, remain to be explored. Here we identify an enhancer-associated lncRNA that enhances eNOS expression (LEENE). Combining RNA-sequencing and chromatin conformation capture methods, we demonstrate that LEENE is co-regulated with eNOS and that its enhancer resides in proximity to eNOS promoter in endothelial cells (ECs). Gain- and Loss-of-function of LEENE differentially regulate eNOS expression and EC function. Mechanistically, LEENE facilitates the recruitment of RNA Pol II to the eNOS promoter to enhance eNOS nascent RNA transcription. Our findings unravel a new layer in eNOS regulation and provide novel insights into cardiovascular regulation involving endothelial function.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Elementos Facilitadores Genéticos/genética
Regulação Enzimológica da Expressão Gênica
Óxido Nítrico Sintase Tipo III/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Perfilação da Expressão Gênica
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Óxido Nítrico Sintase Tipo III/metabolismo
Regiões Promotoras Genéticas/genética
RNA Polimerase II/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Long Noncoding); 0 (long non-coding RNA LEENE, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02113-y


  9 / 127181 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29480845
[Au] Autor:Zhang J; Zhang Y; Zhang Z
[Ad] Endereço:Department of Gynecology and Obstetrics, Capital Medical University affiliated Beijing Chaoyang Hospital, Beijing, China.
[Ti] Título:Association of rs2279744 and rs117039649 promoter polymorphism with the risk of gynecological cancer: A meta-analysis of case-control studies.
[So] Source:Medicine (Baltimore);97(2):e9554, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Increasing evidence has suggested that rs2279744 is associated with rs117039649 polymorphism, which can increase the risk of gynecological cancers, including cervical, ovarian, breast, and endometrial cancer. The results are inconsistent so that we performed a meta-analysis of current literature to clarify the impacts of these polymorphisms on gynecological cancer. METHODS: Eligible articles were identified through an exhaustive search of relevant databases including PubMed, Embase, Web of science, Springer Link, Chinese National Knowledge Infrastructure (CNKI), and Weipu database for the period up to July 2016. Data about the association between single nucleotide polymorphisms (SNPs) and cancer risk were refined from the selected articles as well as other information about cases and controls, and all of them were extracted by 2 independent researchers and pooled odds ratio with 95% confidence interval was calculated. RESULTS: This analysis included 24 articles, 27 case-control studies of rs2279744 polymorphism and 3 case-control studies of rs117039649 polymorphism. Significant association with the risk of gynecological cancer was observed for both SNPs. Subgroup analysis by ethnicity and cancer type (cervical, ovarian, breast, and endometrial) also showed a positive relationship between rs2279744 polymorphism and gynecological cancer risk in Caucasian; and there was also a notable association between rs2279744 polymorphism and cervical cancer. CONCLUSIONS: We found that rs2279744 (SNP309) and rs117039649 (SNP285) were both associated with the risk of gynecological cancers. Subgroup analysis showed that rs2279744 (SNP309) was associated with the risk of gynecological cancers in Caucasian and Asian according to the ethnicity and cancer type, especially for endometrial cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias do Endométrio/genética
Predisposição Genética para Doença
Neoplasias Ovarianas/genética
Proteínas Proto-Oncogênicas c-mdm2/genética
Neoplasias do Colo do Útero/genética
[Mh] Termos MeSH secundário: Neoplasias da Mama/etnologia
Neoplasias do Endométrio/etnologia
Feminino
Seres Humanos
Neoplasias Ovarianas/etnologia
Polimorfismo de Nucleotídeo Único
Regiões Promotoras Genéticas
Neoplasias do Colo do Útero/etnologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
EC 2.3.2.27 (MDM2 protein, human); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009554


  10 / 127181 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29339738
[Au] Autor:Luo N; Nixon MJ; Gonzalez-Ericsson PI; Sanchez V; Opalenik SR; Li H; Zahnow CA; Nickels ML; Liu F; Tantawy MN; Sanders ME; Manning HC; Balko JM
[Ad] Endereço:Department of Anatomy and Histology, School of Medicine, Nankai University, Tianjin, 300071, China.
[Ti] Título:DNA methyltransferase inhibition upregulates MHC-I to potentiate cytotoxic T lymphocyte responses in breast cancer.
[So] Source:Nat Commun;9(1):248, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Potentiating anti-tumor immunity by inducing tumor inflammation and T cell-mediated responses are a promising area of cancer therapy. Immunomodulatory agents that promote these effects function via a wide variety of mechanisms, including upregulation of antigen presentation pathways. Here, we show that major histocompatibility class-I (MHC-I) genes are methylated in human breast cancers, suppressing their expression. Treatment of breast cancer cell lines with a next-generation hypomethylating agent, guadecitabine, upregulates MHC-I expression in response to interferon-γ. In murine tumor models of breast cancer, guadecitabine upregulates MHC-I in tumor cells promoting recruitment of CD8+ T cells to the microenvironment. Finally, we show that MHC-I genes are upregulated in breast cancer patients treated with hypomethylating agents. Thus, the immunomodulatory effects of hypomethylating agents likely involve upregulation of class-I antigen presentation to potentiate CD8+ T cell responses. These strategies may be useful to potentiate anti-tumor immunity and responses to checkpoint inhibition in immune-refractory breast cancers.
[Mh] Termos MeSH primário: Azacitidina/análogos & derivados
Neoplasias da Mama/metabolismo
DNA (Citosina-5-)-Metiltransferase 1/antagonistas & inibidores
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Genes MHC Classe I/fisiologia
Linfócitos T Citotóxicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Azacitidina/farmacologia
Linhagem Celular Tumoral
DNA (Citosina-5-)-Metiltransferase 1/genética
DNA (Citosina-5-)-Metiltransferase 1/metabolismo
Feminino
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Genes MHC Classe I/genética
Seres Humanos
Neoplasias Mamárias Experimentais
Camundongos
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 2KT4YN1DP7 (guadecitabine); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNMT1 protein, human); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02630-w



página 1 de 12719 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde