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Pesquisa : G05.360.340.024.340.220 [Categoria DeCS]
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[PMID]:28912064
[Au] Autor:Zhu Y; Li B; Wu T; Ye L; Zeng Y; Zhang Y
[Ad] Endereço:School of Life Sciences, Tsinghua University, Beijing, China; Key Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.
[Ti] Título:Cell cycle and histone modification genes were decreased in placenta tissue from unexplained early miscarriage.
[So] Source:Gene;636:17-22, 2017 Dec 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Genetic defect is a major cause of early miscarriage, but still in many cases the etiology are not fully understood. Recent studies have shown that dysregulation of genes in placenta tissue are participated in the pathogenesis of unexplained early miscarriage. The aim of our study is to explore mRNA expression profile in placental chorionic villi and to reveal the underlying mechanism of unexplained early miscarriage. Chorionic villous were isolated and extracted from early miscarriage (n=3) and control pregnancy (n=3) placenta with normal chromosome karyotype using MLPA assay, and then mRNA expression profiles were determined by microarray. For verification the reproducibility of the microarray, three up-regulated genes and six down-regulated genes were chosen and examined by real-time PCR (n=30). A total of 81 genes were up-regulated and 231 genes were down-regulated when compared to the control group, and the differences were reached statistically significances (P<0.05). After Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, we found that almost down-regulation genes are associated with cell cycle and histone modification, and these genes are participated in several important physiological processes, such as cell proliferation, nuclear division, chromatic assembly, DNA packing and modification. These results indicated that cell cycle and histone modification genes, and related signaling pathway maybe contribute to the genesis and development of unexplained early miscarriage. Further studies and validations are necessary to elucidate the exact roles of these genes in miscarriage pathogenesis, which can develop tools for early detection and management.
[Mh] Termos MeSH primário: Aborto Espontâneo/genética
Genes cdc
Código das Histonas/genética
Placenta/metabolismo
[Mh] Termos MeSH secundário: Aborto Espontâneo/metabolismo
Vilosidades Coriônicas/metabolismo
Feminino
Regulação da Expressão Gênica
Ontologia Genética
Seres Humanos
Gravidez
Mapas de Interação de Proteínas
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE


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[PMID]:28807995
[Au] Autor:Matsuda S; Hammaker D; Topolewski K; Briegel KJ; Boyle DL; Dowdy S; Wang W; Firestein GS
[Ad] Endereço:Division of Rheumatology, Allergy and Immunology, University of California San Diego School of Medicine, La Jolla, CA 92093.
[Ti] Título:Regulation of the Cell Cycle and Inflammatory Arthritis by the Transcription Cofactor Gene.
[So] Source:J Immunol;199(7):2316-2322, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) display unique aggressive behavior, invading the articular cartilage and promoting inflammation. Using an integrative analysis of RA risk alleles, the transcriptome and methylome in RA FLS, we recently identified the limb bud and heart development ( ) gene as a key dysregulated gene in RA and other autoimmune diseases. Although some evidence suggests that LBH could modulate the cell cycle, the precise mechanism is unknown and its impact on inflammation in vivo has not been defined. Our cell cycle analysis studies show that LBH deficiency in FLS leads to S-phase arrest and failure to progress through the cell cycle. LBH-deficient FLS had increased DNA damage and reduced expression of the catalytic subunit of DNA polymerase α. Decreased DNA polymerase α was followed by checkpoint arrest due to phosphorylation of checkpoint kinase 1. Because DNA fragments can increase arthritis severity in preclinical models, we then explored the effect of LBH deficiency in the K/BxN serum transfer model. knockout exacerbated disease severity, which is associated with elevated levels of IL-1ß and checkpoint kinase 1 phosphorylation. These studies indicate that LBH deficiency induces S-phase arrest that, in turn, exacerbates inflammation. Because gene variants are associated with type I diabetes mellitus, systemic lupus erythematosus, RA, and celiac disease, these results suggest a general mechanism that could contribute to immune-mediated diseases.
[Mh] Termos MeSH primário: Artrite Reumatoide/genética
Ciclo Celular/genética
Proteínas Nucleares/genética
Sinoviócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Artrite Experimental
Artrite Reumatoide/imunologia
Artrite Reumatoide/fisiopatologia
Células Cultivadas
Quinase do Ponto de Checagem 1/genética
Dano ao DNA
DNA Polimerase I/genética
DNA Polimerase I/metabolismo
Regulação da Expressão Gênica
Genes cdc
Seres Humanos
Interleucina-1beta/biossíntese
Camundongos
Camundongos Knockout
Proteínas Nucleares/deficiência
Proteínas Nucleares/metabolismo
Fosforilação
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Lbh protein, mouse); 0 (Nuclear Proteins); EC 2.7.11.1 (Checkpoint Kinase 1); EC 2.7.11.1 (Chek1 protein, mouse); EC 2.7.7.- (DNA Polymerase I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700719


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[PMID]:28694034
[Au] Autor:Turajlic S; Litchfield K; Xu H; Rosenthal R; McGranahan N; Reading JL; Wong YNS; Rowan A; Kanu N; Al Bakir M; Chambers T; Salgado R; Savas P; Loi S; Birkbak NJ; Sansregret L; Gore M; Larkin J; Quezada SA; Swanton C
[Ad] Endereço:Translational Cancer Therapeutics Laboratory, The Francis Crick Institute, London, UK; Renal and Skin Units, The Royal Marsden Hospital National Health Service Foundation Trust, London, UK.
[Ti] Título:Insertion-and-deletion-derived tumour-specific neoantigens and the immunogenic phenotype: a pan-cancer analysis.
[So] Source:Lancet Oncol;18(8):1009-1021, 2017 Aug.
[Is] ISSN:1474-5488
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The focus of tumour-specific antigen analyses has been on single nucleotide variants (SNVs), with the contribution of small insertions and deletions (indels) less well characterised. We investigated whether the frameshift nature of indel mutations, which create novel open reading frames and a large quantity of mutagenic peptides highly distinct from self, might contribute to the immunogenic phenotype. METHODS: We analysed whole-exome sequencing data from 5777 solid tumours, spanning 19 cancer types from The Cancer Genome Atlas. We compared the proportion and number of indels across the cohort, with a subset of results replicated in two independent datasets. We assessed in-silico tumour-specific neoantigen predictions by mutation type with pan-cancer analysis, together with RNAseq profiling in renal clear cell carcinoma cases (n=392), to compare immune gene expression across patient subgroups. Associations between indel burden and treatment response were assessed across four checkpoint inhibitor datasets. FINDINGS: We observed renal cell carcinomas to have the highest proportion (0·12) and number of indel mutations across the pan-cancer cohort (p<2·2 × 10 ), more than double the median proportion of indel mutations in all other cancer types examined. Analysis of tumour-specific neoantigens showed that enrichment of indel mutations for high-affinity binders was three times that of non-synonymous SNV mutations. Furthermore, neoantigens derived from indel mutations were nine times enriched for mutant specific binding, as compared with non-synonymous SNV derived neoantigens. Immune gene expression analysis in the renal clear cell carcinoma cohort showed that the presence of mutant-specific neoantigens was associated with upregulation of antigen presentation genes, which correlated (r=0·78) with T-cell activation as measured by CD8-positive expression. Finally, analysis of checkpoint inhibitor response data revealed frameshift indel count to be significantly associated with checkpoint inhibitor response across three separate melanoma cohorts (p=4·7 × 10 ). INTERPRETATION: Renal cell carcinomas have the highest pan-cancer proportion and number of indel mutations. Evidence suggests indels are a highly immunogenic mutational class, which can trigger an increased abundance of neoantigens and greater mutant-binding specificity. FUNDING: Cancer Research UK, UK National Institute for Health Research (NIHR) at the Royal Marsden Hospital National Health Service Foundation Trust, Institute of Cancer Research and University College London Hospitals Biomedical Research Centres, the UK Medical Research Council, the Rosetrees Trust, Novo Nordisk Foundation, the Prostate Cancer Foundation, the Breast Cancer Research Foundation, the European Research Council.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/genética
DNA de Neoplasias/análise
Mutação da Fase de Leitura
Mutação INDEL
Neoplasias/genética
Neoplasias/imunologia
[Mh] Termos MeSH secundário: Linfócitos T CD8-Positivos
Carcinoma de Células Renais/genética
Carcinoma de Células Renais/imunologia
Análise Mutacional de DNA
Bases de Dados Genéticas
Exoma
Genes cdc
Genômica
Seres Humanos
Neoplasias Renais/genética
Neoplasias Renais/imunologia
Ativação Linfocitária/genética
Melanoma/genética
Melanoma/imunologia
Fenótipo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (DNA, Neoplasm)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


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[PMID]:28683958
[Au] Autor:Jacquin-Porretaz C; Nardin C; Puzenat E; Roche-Kubler B; Aubin F; Comité de suivi des effets secondaires des immunothérapies anti-cancéreuses(CSESIAC)
[Ad] Endereço:CHU de Besançon, service de dermatologie, 25030 Besançon France.
[Ti] Título:[Adverse effects of immune checkpoint inhibitors used to treat melanoma and other cancer].
[Ti] Título:Effets secondaires des inhibiteurs de checkpoint utilisés dans le traitement des mélanomes et d'autres cancers..
[So] Source:Presse Med;46(9):808-817, 2017 Sep.
[Is] ISSN:2213-0276
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Monoclonal antibodies targeted against the immune checkpoint molecules CTLA-4 and PD-1 have recently obtained approval for the treatment of metastatic melanoma and advanced/refractory non small-cell lung cancers and metastatic renal cancer. Besides their efficacy profile, these immune targeted agents also generate immune-related adverse events that may be life threatening if not anticipated and managed appropriately. This new family of dysimmune toxicities remains largely unknown to the broad oncology community. We propose here some practical guidelines for the oncologist to help in the clinical care of patients under immune checkpoint molecules.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Antígeno CTLA-4/antagonistas & inibidores
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma de Células Renais/tratamento farmacológico
Carcinoma de Células Renais/genética
Genes cdc/efeitos dos fármacos
Imunotoxinas/efeitos adversos
Imunotoxinas/uso terapêutico
Neoplasias Renais/tratamento farmacológico
Neoplasias Renais/genética
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Melanoma/tratamento farmacológico
Melanoma/genética
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Antígeno CTLA-4/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Carcinoma de Células Renais/patologia
Fidelidade a Diretrizes
Neoplasias Renais/patologia
Neoplasias Pulmonares/patologia
Metástase Neoplásica
Receptor de Morte Celular Programada 1/genética
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (Immunotoxins); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


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[PMID]:28639883
[Au] Autor:Sell S
[Ad] Endereço:Wadsworth Center, New York State Department of Health and Albany College of Pharmacy and Health Sciences, Albany, NY, USA.
[Ti] Título:Cancer immunotherapy: Breakthrough or "deja vu, all over again"?
[So] Source:Tumour Biol;39(6):1010428317707764, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:From the application of Coley's toxin in the early 1900s to the present clinical trials using immune checkpoint regulatory inhibitors, the history of cancer immunotherapy has consisted of extremely high levels of enthusiasm after anecdotal case reports of enormous success, followed by decreasing levels of enthusiasm as the results of controlled clinical trials are available. In this review, this pattern will be documented for the various immunotherapeutic approaches over the years. The sole exception being vaccination against cancer causing viruses, which have already prevented thousands of cancers. We can only hope that the present high level of enthusiasm for the use of immune stimulation by removal of blocks to cancer immunity will be more productive than the incremental improvements using previous immunotherapies.
[Mh] Termos MeSH primário: Vacinas Anticâncer/uso terapêutico
Imunoterapia
Neoplasias/imunologia
Neoplasias/terapia
[Mh] Termos MeSH secundário: Vacinas Anticâncer/imunologia
Genes cdc/imunologia
Seres Humanos
Neoplasias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cancer Vaccines)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317707764


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[PMID]:28285642
[Au] Autor:Dogan A; Demirci S; Apdik H; Bayrak OF; Gulluoglu S; Tuysuz EC; Gusev O; Rizvanov AA; Nikerel E; Sahin F
[Ad] Endereço:Department of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755 Atasehir, Istanbul, Turkey; National Cancer Institute, CDBL, NIH, Frederick, MD.
[Ti] Título:A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/ß-catenin pathway.
[So] Source:Metabolism;69:130-142, 2017 Apr.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity is a worldwide medical problem resulting in serious morbidity and mortality involving differentiation of pre-adipocytes into mature adipocytes (adipogenesis). Boron treatment has been reported to be associated with weight reduction in experimental animals; however, its effects on pre-adipocyte differentiation and anti-adipogenic molecular mechanisms are unknown. In this study, we demonstrate the inhibitory activities of boric acid (BA) and sodium pentaborate pentahydrate (NaB) on adipogenesis using common cellular models. Boron treatment repressed the expression of adipogenesis-related genes and proteins, including CCAAT-enhancer-binding protein α and peroxisome proliferator-activated receptor γ, by regulating critical growth factors and the ß-catenin, AKT, and extracellular signal-regulated kinase signaling pathways. In addition, although boron treatment did not induce apoptosis in pre-adipocytes, it depressed mitotic clonal expansion by regulation of cell cycle genes. Overall, these data offer promising insights into the prevention/treatment of obesity and associated diseases.
[Mh] Termos MeSH primário: Adipogenia/efeitos dos fármacos
Fármacos Antiobesidade/uso terapêutico
Compostos de Boro/farmacologia
Obesidade/tratamento farmacológico
Células-Tronco/efeitos dos fármacos
Via de Sinalização Wnt/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/efeitos dos fármacos
Adipogenia/genética
Adiponectina/biossíntese
Adiponectina/genética
Animais
Boratos/farmacologia
Ácidos Bóricos/farmacologia
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Citocinas/biossíntese
Citocinas/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Genes cdc/efeitos dos fármacos
Leptina/biossíntese
Leptina/genética
Camundongos
Mitose/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Adipoq protein, mouse); 0 (Anti-Obesity Agents); 0 (Borates); 0 (Boric Acids); 0 (Boron Compounds); 0 (Cytokines); 0 (Leptin); 0 (sodium pentaborate); R57ZHV85D4 (boric acid)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE


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[PMID]:28276698
[Au] Autor:Sgambato A; Casaluce F; Gridelli C
[Ad] Endereço:a Division of Medical Oncology , 'S. G. Moscati' Hospital , Avellino , Italy.
[Ti] Título:The role of checkpoint inhibitors immunotherapy in advanced non-small cell lung cancer in the elderly.
[So] Source:Expert Opin Biol Ther;17(5):565-571, 2017 May.
[Is] ISSN:1744-7682
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Immune checkpoint inhibition is a novel treatment modality that has brought a new hope to patients with advanced NSCLC. Several molecules targeting cytotoxic T-lymphocyte antigen 4 (CTLA4) or programmed cell death 1 receptor/programmed death ligand-1 (PD1/PD-L1) pathways are under evaluation in NSCLC and three of them are currently approved: nivolumab and atezolizumab for advanced NSCLC after prior chemotherapy and pembrolizumab for advanced NSCLC expressing PD-L1 ≥ 1% after at least one prior chemotherapy regimen and > 50% as a first-line response. Areas covered: To date, the efficacy and toxicity of immune checkpoint inhibitors in the elderly is unclear because available studies involved mainly a low number of elderly patients. In this paper, the authors discuss the frailty of the elderly patient and the challenges of choosing the best therapeutic strategy, focusing on the role of immune checkpoint inhibitors. Expert opinion: There are several outstanding goals that need to be met for the proper and safe use of immunotherapeutic drugs. In terms of the elderly, it is true that age-tailored clinical trials are needed to confirm the real impact of immunotherapy and harmonize the standard of care in this specific demographic.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/terapia
Genes cdc/efeitos dos fármacos
Imunoterapia/métodos
Neoplasias Pulmonares/terapia
[Mh] Termos MeSH secundário: Idoso
Envelhecimento/efeitos dos fármacos
Envelhecimento/imunologia
Animais
Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/imunologia
Anticorpos Monoclonais Humanizados/administração & dosagem
Anticorpos Monoclonais Humanizados/imunologia
Antígeno B7-H1/antagonistas & inibidores
Antígeno B7-H1/imunologia
Antígeno CTLA-4/antagonistas & inibidores
Antígeno CTLA-4/imunologia
Carcinoma Pulmonar de Células não Pequenas/diagnóstico
Carcinoma Pulmonar de Células não Pequenas/imunologia
Genes cdc/imunologia
Seres Humanos
Neoplasias Pulmonares/diagnóstico
Neoplasias Pulmonares/imunologia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptor de Morte Celular Programada 1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (B7-H1 Antigen); 0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (Programmed Cell Death 1 Receptor); 31YO63LBSN (nivolumab); DPT0O3T46P (pembrolizumab)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/14712598.2017.1294157


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[PMID]:28252645
[Au] Autor:Thole TM; Lodrini M; Fabian J; Wuenschel J; Pfeil S; Hielscher T; Kopp-Schneider A; Heinicke U; Fulda S; Witt O; Eggert A; Fischer M; Deubzer HE
[Ad] Endereço:Department of Pediatric Hematology, Oncology and SCT, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, Berlin 13353, Germany.
[Ti] Título:Neuroblastoma cells depend on HDAC11 for mitotic cell cycle progression and survival.
[So] Source:Cell Death Dis;8(3):e2635, 2017 Mar 02.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The number of long-term survivors of high-risk neuroblastoma remains discouraging, with 10-year survival as low as 20%, despite decades of considerable international efforts to improve outcome. Major obstacles remain and include managing resistance to induction therapy, which causes tumor progression and early death in high-risk patients, and managing chemotherapy-resistant relapses, which can occur years after the initial diagnosis. Identifying and validating novel therapeutic targets is essential to improve treatment. Delineating and deciphering specific functions of single histone deacetylases in neuroblastoma may support development of targeted acetylome-modifying therapeutics for patients with molecularly defined high-risk neuroblastoma profiles. We show here that HDAC11 depletion in MYCN-driven neuroblastoma cell lines strongly induces cell death, mostly mediated by apoptotic programs. Genes necessary for mitotic cell cycle progression and cell division were most prominently enriched in at least two of three time points in whole-genome expression data combined from two cell systems, and all nine genes in these functional categories were strongly repressed, including CENPA, KIF14, KIF23 and RACGAP1. Enforced expression of one selected candidate, RACGAP1, partially rescued the induction of apoptosis caused by HDAC11 depletion. High-level expression of all nine genes in primary neuroblastomas significantly correlated with unfavorable overall and event-free survival in patients, suggesting a role in mediating the more aggressive biological and clinical phenotype of these tumors. Our study identified a group of cell cycle-promoting genes regulated by HDAC11, being both predictors of unfavorable patient outcome and essential for tumor cell viability. The data indicate a significant role of HDAC11 for mitotic cell cycle progression and survival of MYCN-amplified neuroblastoma cells, and suggests that HDAC11 could be a valuable drug target.
[Mh] Termos MeSH primário: Ciclo Celular/genética
Sobrevivência Celular/genética
Histona Desacetilases/metabolismo
Mitose/genética
Neuroblastoma/genética
Neuroblastoma/metabolismo
[Mh] Termos MeSH secundário: Apoptose/genética
Linhagem Celular Tumoral
Intervalo Livre de Doença
Expressão Gênica/genética
Genes cdc/genética
Seres Humanos
Recidiva Local de Neoplasia/genética
Recidiva Local de Neoplasia/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.5.1.98 (HDAC11 protein, human); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.49


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[PMID]:28164687
[Au] Autor:Xu J; Zhao J; Liu F; Zhang R
[Ad] Endereço:Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital, Shenyang, China.
[Ti] Título:Analysis of mechanism and feature genes of colorectal cancer by bioinformatic methods.
[So] Source:Minerva Med;108(1):94-95, 2017 Feb.
[Is] ISSN:1827-1669
[Cp] País de publicação:Italy
[La] Idioma:eng
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Neoplasias Colorretais/genética
Genes Neoplásicos
[Mh] Termos MeSH secundário: Quimiocinas/genética
Progressão da Doença
Perfilação da Expressão Gênica
Ontologia Genética
Genes cdc
Seres Humanos
Proteínas de Neoplasias/genética
Análise de Sequência com Séries de Oligonucleotídeos
RNA Neoplásico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Neoplasm Proteins); 0 (RNA, Neoplasm)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.23736/S0026-4806.16.04611-5


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[PMID]:26892570
[Au] Autor:Nan P; Yan S; Wang Y; Du Q; Chang Z
[Ad] Endereço:Molecular and Genetic Laboratory, College of Life Science, Henan Normal University, No.46, East Jianshe Road, Xinxiang, Henan, 453007, China.
[Ti] Título:Gene expression profile changes induced by acute toxicity of [C mim]Cl in loach (Paramisgurnus dabryanus).
[So] Source:Environ Toxicol;32(2):404-416, 2017 Feb.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ionic liquids (ILs) are widely used as reaction media in various commercial applications. Many reports have indicated that most ILs are poorly decomposed by microorganisms and are toxic to aquatic organisms. In this study, differential gene expression profiling was conducted using a suppression subtraction hybridization cDNA library from hepatic tissue of the loach (Paramisgurnus dabryanus) after exposure to 1-hexadecyl-3-methylimidazolium chloride ([C mim]Cl), a representative IL. Two hundred and fifty-nine differentially expressed candidate genes, whose expression was altered by >2.0-fold by the [C mim]Cl treatment, were identified, including 127 upregulated genes and 132 downregulated genes. A gene ontology analysis of the known genes isolated in this study showed that [C mim]Cl-responsive genes were involved in cell cycle, stimulus response, defense response, DNA damage response, oxidative stress responses, and other biological responses. To identify candidate genes that may be involved in [C mim]Cl-induced toxicity, 259 clones were examined by Southern blot macroarray hybridization, and 20 genes were further characterized using quantitative real-time polymerase chain reaction. Finally, six candidate genes were selected, including three DNA damage response genes, two toxic substance metabolic genes, and one stress protein gene. Our results indicate that these changes in gene expression are associated with [C mim]Cl-induced toxicity, and that these six candidate genes can be promising biomarkers for detecting [C mim]Cl-induced toxicity. Therefore, this study demonstrates the use of a powerful assay to identify genes potentially involved in [C mim]Cl toxicity, and it provides a foundation for the further study of related genes and the molecular mechanism of [C mim]Cl toxicity. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 404-416, 2017.
[Mh] Termos MeSH primário: Cipriniformes/genética
Expressão Gênica/efeitos dos fármacos
Imidazóis/toxicidade
Líquidos Iônicos/toxicidade
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Dano ao DNA
DNA Complementar/biossíntese
DNA Complementar/genética
Perfilação da Expressão Gênica
Genes cdc/efeitos dos fármacos
Proteínas de Choque Térmico/efeitos dos fármacos
Proteínas de Choque Térmico/genética
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/genética
RNA/biossíntese
RNA/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-hexadecyl-3-methylimidazolium chloride); 0 (Biomarkers); 0 (DNA, Complementary); 0 (Heat-Shock Proteins); 0 (Imidazoles); 0 (Ionic Liquids); 63231-63-0 (RNA)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160220
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22244



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