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Pesquisa : D08.811.913.696.620.682.700.125.387 [Categoria DeCS]
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[PMID]:28743390
[Au] Autor:Li S; Sun X; Xu L; Sun R; Ma Z; Deng X; Liu B; Fu Q; Qu R; Ma S
[Ad] Endereço:Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 639, Longmian Road, Nanjing 211198, China; Jiangsu Provincial Key Laboratory for TCM Evaluation and Translational Research, China Pharmaceutical University, 639, Longmian Road, Nanjing 211198, China.
[Ti] Título:Baicalin attenuates in vivo and in vitro hyperglycemia-exacerbated ischemia/reperfusion injury by regulating mitochondrial function in a manner dependent on AMPK.
[So] Source:Eur J Pharmacol;815:118-126, 2017 Nov 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cerebral ischemia/reperfusion (I/R) is a lethal and disabling disease. Studies have suggested that hyperglycemia is a risk factor for cerebral I/R. Baicalin is a natural bioactive flavonoid extracted from Scutellaria baicalensis Georgi with neuroprotective activity. In the present study, we investigated the effects of baicalin on hyperglycemia-exacerbated cerebral I/R injury. Streptozotocin (STZ) injection aggravated the brain damage induced by middle cerebral artery occlusion (MCAO) surgery, while baicalin administration reduced blood glucose, relieved neurological deficit and decreased infarct volume. In vitro, Oxygen-glucose deprivation/ reperfusion (OGD/REP) induced inordinate reactive oxygen species (ROS) production and mitochondrial dynamic impairments were markedly increased under high glucose (HG) condition. Baicalin treatment in PC12 cells inhibited dynamin-related protein 1 (Drp-1) expression, decreased mitochondrial fission, promoted mitofusin-2 (MFN2) generation, increased Drp-1 Ser637 phosphorylation, and elevated mitochondrial membrane potential (Δψm) via the suppression of ROS production. However, AMPKα1 knockdown abolished the protective effects of baicalin. Baicalin also suppressed cell apoptosis and enhanced mitophagy. These results suggested that baicalin protected against hyperglycemia aggravated I/R injury by regulating mitochondrial functions in a manner dependent on AMPK.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Flavonoides/farmacologia
Hiperglicemia/complicações
Mitocôndrias/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteínas Quinases Associadas com Morte Celular/metabolismo
Ativação Enzimática/efeitos dos fármacos
Flavonoides/uso terapêutico
Infarto da Artéria Cerebral Média/complicações
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Membrana/metabolismo
Mitocôndrias/patologia
Dinâmica Mitocondrial/efeitos dos fármacos
Proteínas Mitocondriais/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurônios/patologia
Fármacos Neuroprotetores/uso terapêutico
Células PC12
Fosforilação/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Traumatismo por Reperfusão/complicações
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flavonoids); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Neuroprotective Agents); 0 (Reactive Oxygen Species); 0 (mitofusin 2 protein, rat); 347Q89U4M5 (baicalin); EC 2.7.11.1 (Death-Associated Protein Kinases); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28934284
[Au] Autor:Yuan W; Chen J; Shu Y; Liu S; Wu L; Ji J; Liu Z; Tang Q; Zhou Z; Cheng Y; Jiang B; Shu X
[Ad] Endereço:Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Correlation of DAPK1 methylation and the risk of gastrointestinal cancer: A systematic review and meta-analysis.
[So] Source:PLoS One;12(9):e0184959, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: One of the critical mechanisms of gastrointestinal cancer pathogenesis is the silencing of death associated protein kinase 1 (DAPK1), which could be caused by aberrant methylation of the promoter. However, the relationship between DAPK1 methylation and the risk of gastrointestinal cancer is still controversial. Hence, we conducted this study to determine the potential correlation. METHODS: Eligible publications were searched in the Pubmed, Embase, and Cochrane Library through November 2016 according to the inclusion criteria and exclusion criteria. Revman 5.3 and Stata 12.0 software were used to analyze the relevant data regarding the association between the frequency of DAPK1 methylation and gastrointestinal cancer. RESULTS: A total of 22 studies with 2406 patients were included in this meta analysis. Methylation of DAPK1 was positively related with the risk of gastrointestinal cancer (odds ratio [OR] = 5.35, 95% confidence interval [CI]: 2.76-10.38, P<0.00001, random effects model). The source of heterogeneity was analyzed by sensitivity analysis and subgroup analysis. After omitting one heterogeneous study, the I2 decreased and the OR increased in pooled analysis. Also, the heterogeneity decreased most significantly in the subgroup of studies that had a sample size of less than 60 cases. Then, the correlations between DAPK1 methylation and clinicopathological features of gastrointestinal cancer were assessed. DAPK1 methylation was positively correlated with the lymph node (N) stage (positive vs. negative, OR = 1.45, 95%CI: 1.01-2.06, P = 0.04, fixed effects model) and poor differentiation (OR = 1.55, 95%CI: 1.02-2.35, P = 0.04, fixed effects model) in gastric cancer, and the association was significant among Asian patients. However, among cases of gastrointestinal cancer, the association between DAPK1 methylation and tumor (T) stage, N stage, distant metastasis (M) stage, and cancer differentiation were not statistically significant. CONCLUSIONS: DAPK1 methylation is a potential biomarker for the early diagnosis of gastrointestinal cancer. Further analysis of the clinicopathological features indicated that aberrant methylation of DAPK1 is positively associated with the tumorigenesis of gastrointestinal cancer, and metastasis of gastric cancer.
[Mh] Termos MeSH primário: Metilação de DNA
Proteínas Quinases Associadas com Morte Celular/genética
Neoplasias Gastrointestinais/genética
Predisposição Genética para Doença
[Mh] Termos MeSH secundário: Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
EC 2.7.11.1 (DAPK1 protein, human); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184959


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[PMID]:28617226
[Au] Autor:Tran HJ; Speyer G; Kiefer J; Kim S
[Ad] Endereço:Integrated Cancer Genomics Division, The Translational Genomics Research Institute, Phoenix, AZ, 85004, USA.
[Ti] Título:Contextualization of drug-mediator relations using evidence networks.
[So] Source:BMC Bioinformatics;18(Suppl 7):252, 2017 May 31.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Genomic analysis of drug response can provide unique insights into therapies that can be used to match the "right drug to the right patient." However, the process of discovering such therapeutic insights using genomic data is not straightforward and represents an area of active investigation. EDDY (Evaluation of Differential DependencY), a statistical test to detect differential statistical dependencies, is one method that leverages genomic data to identify differential genetic dependencies. EDDY has been used in conjunction with the Cancer Therapeutics Response Portal (CTRP), a dataset with drug-response measurements for more than 400 small molecules, and RNAseq data of cell lines in the Cancer Cell Line Encyclopedia (CCLE) to find potential drug-mediator pairs. Mediators were identified as genes that showed significant change in genetic statistical dependencies within annotated pathways between drug sensitive and drug non-sensitive cell lines, and the results are presented as a public web-portal (EDDY-CTRP). However, the interpretability of drug-mediator pairs currently hinders further exploration of these potentially valuable results. METHODS: In this study, we address this challenge by constructing evidence networks built with protein and drug interactions from the STITCH and STRING interaction databases. STITCH and STRING are sister databases that catalog known and predicted drug-protein interactions and protein-protein interactions, respectively. Using these two databases, we have developed a method to construct evidence networks to "explain" the relation between a drug and a mediator.  RESULTS: We applied this approach to drug-mediator relations discovered in EDDY-CTRP analysis and identified evidence networks for ~70% of drug-mediator pairs where most mediators were not known direct targets for the drug. Constructed evidence networks enable researchers to contextualize the drug-mediator pair with current research and knowledge. Using evidence networks, we were able to improve the interpretability of the EDDY-CTRP results by linking the drugs and mediators with genes associated with both the drug and the mediator. CONCLUSION: We anticipate that these evidence networks will help inform EDDY-CTRP results and enhance the generation of important insights to drug sensitivity that will lead to improved precision medicine applications.
[Mh] Termos MeSH primário: Preparações Farmacêuticas/metabolismo
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Ciclina H/química
Ciclina H/genética
Ciclina H/metabolismo
Reparo do DNA
Bases de Dados Factuais
Proteínas Quinases Associadas com Morte Celular/química
Proteínas Quinases Associadas com Morte Celular/genética
Proteínas Quinases Associadas com Morte Celular/metabolismo
Redes Reguladoras de Genes
Seres Humanos
Imidazóis/química
Imidazóis/metabolismo
Preparações Farmacêuticas/química
Inibidores de Proteínas Quinases/química
Inibidores de Proteínas Quinases/metabolismo
Proteínas Serina-Treonina Quinases/química
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas/química
Proteínas/genética
Triazinas/química
Triazinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin H); 0 (Imidazoles); 0 (OSI 027); 0 (Pharmaceutical Preparations); 0 (Protein Kinase Inhibitors); 0 (Proteins); 0 (Triazines); EC 2.7.11.1 (DAPK3 protein, human); EC 2.7.11.1 (Death-Associated Protein Kinases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (STK33 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-017-1642-8


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[PMID]:28604729
[Au] Autor:Brocks D; Schmidt CR; Daskalakis M; Jang HS; Shah NM; Li D; Li J; Zhang B; Hou Y; Laudato S; Lipka DB; Schott J; Bierhoff H; Assenov Y; Helf M; Ressnerova A; Islam MS; Lindroth AM; Haas S; Essers M; Imbusch CD; Brors B; Oehme I; Witt O; Lübbert M; Mallm JP; Rippe K; Will R; Weichenhan D; Stoecklin G; Gerhäuser C; Oakes CC; Wang T; Plass C
[Ad] Endereço:Division of Epigenomics and Cancer Risk Factors, DKFZ, Heidelberg, Germany.
[Ti] Título:DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats.
[So] Source:Nat Genet;49(7):1052-1060, 2017 Jul.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several mechanisms of action have been proposed for DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi), primarily based on candidate-gene approaches. However, less is known about their genome-wide transcriptional and epigenomic consequences. By mapping global transcription start site (TSS) and chromatin dynamics, we observed the cryptic transcription of thousands of treatment-induced non-annotated TSSs (TINATs) following DNMTi and HDACi treatment. The resulting transcripts frequently splice into protein-coding exons and encode truncated or chimeric ORFs translated into products with predicted abnormal or immunogenic functions. TINAT transcription after DNMTi treatment coincided with DNA hypomethylation and gain of classical promoter histone marks, while HDACi specifically induced a subset of TINATs in association with H2AK9ac, H3K14ac, and H3K23ac. Despite this mechanistic difference, both inhibitors convergently induced transcription from identical sites, as we found TINATs to be encoded in solitary long terminal repeats of the ERV9/LTR12 family, which are epigenetically repressed in virtually all normal cells.
[Mh] Termos MeSH primário: DNA (Citosina-5-)-Metiltransferases/antagonistas & inibidores
Proteínas Quinases Associadas com Morte Celular/genética
Código das Histonas
Inibidores de Histona Desacetilases/farmacologia
Sequências Repetidas Terminais/genética
Sítio de Iniciação de Transcrição/efeitos dos fármacos
[Mh] Termos MeSH secundário: Processamento Alternativo/genética
Animais
Benzimidazóis/farmacologia
Linhagem Celular Tumoral
DNA (Citosina-5-)-Metiltransferase 1
DNA (Citosina-5-)-Metiltransferases/fisiologia
Metilação de DNA
Proteínas Quinases Associadas com Morte Celular/antagonistas & inibidores
Repressão Epigenética
Éxons/genética
Feminino
Perfilação da Expressão Gênica
Inativação Gênica
Seres Humanos
Ácidos Hidroxâmicos/farmacologia
Íntrons/genética
Camundongos
Camundongos Nus
Interferência de RNA
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Recombinant Fusion Proteins); 0 (SB939 compound); 58IFB293JI (vorinostat); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.7.11.1 (DAPK1 protein, human); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3889


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[PMID]:28543175
[Au] Autor:Li D; Xu D; Xu Y; Chen L; Li C; Dai X; Zhang L; Zheng L
[Ad] Endereço:The Second Hospital of Jilin University, Reproductive Medical Center, Changchun, Jilin, P.R. of China.
[Ti] Título:MicroRNA-141-3p targets DAPK1 and inhibits apoptosis in rat ovarian granulosa cells.
[So] Source:Cell Biochem Funct;35(4):197-201, 2017 Jun.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The polycystic ovary syndrome (PCOS) is a complex and heterogeneous endocrine disorder. MicroRNAs negatively regulate the expression of target genes at posttranscriptional level by binding to the 3' untranslated region of target genes. Our previous study showed that miR-141-3p was dramatically decreased in the ovaries of rat PCOS models. In this study, we aimed to characterize the target of miR-141-3p in rat ovarian granulosa cells. 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay showed that cell viability was dramatically increased when miR-141-3p was overexpressed but was decreased when miR-141-3p was interfered. Flow cytometry showed that cell apoptotic rate was dramatically decreased when miR-141-3p was overexpressed but was increased when miR-141-3p was interfered. Bioinformatics analysis predicted that death-associated protein kinase 1 (DAPK1) might be the target gene of miR-141-3p because the 3' untranslated region of DAPK1 contains sequences complementary to microRNA-141-3p. Transfection with miR-141-3p mimics and inhibitor into granulosa cells showed that both DAPK1 mRNA and protein levels were negatively correlated with miR-141-3p level. Dual-luciferase reporter assay established that DAPK1 was the target of miR-141-3p. Taken together, our data indicate that miR-141-3p may inhibit ovarian granulosa cell apoptosis via targeting DAPK1 and is involved in the etiology of PCOS.
[Mh] Termos MeSH primário: Apoptose
Proteínas Quinases Associadas com Morte Celular/biossíntese
Regulação Enzimológica da Expressão Gênica
Células da Granulosa/metabolismo
MicroRNAs/metabolismo
Síndrome do Ovário Policístico/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Linhagem Celular Transformada
Proteínas Quinases Associadas com Morte Celular/genética
Feminino
Células da Granulosa/patologia
MicroRNAs/genética
Síndrome do Ovário Policístico/genética
Síndrome do Ovário Policístico/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MicroRNAs); 0 (Mirn141 microRNA, rat); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3248


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[PMID]:28436949
[Au] Autor:Vivo M; Fontana R; Ranieri M; Capasso G; Angrisano T; Pollice A; Calabrò V; La Mantia G
[Ad] Endereço:Dipartimento di Biologia, Università Degli Studi di Napoli 'Federico II', Napoli, Italy.
[Ti] Título:p14ARF interacts with the focal adhesion kinase and protects cells from anoikis.
[So] Source:Oncogene;36(34):4913-4928, 2017 Aug 24.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The ARF protein functions as an important sensor of hyper-proliferative stimuli restricting cell proliferation through both p53-dependent and -independent pathways. Although to date the majority of studies on ARF have focused on its anti-proliferative role, few studies have addressed whether ARF may also have pro-survival functions. Here we show for the first time that during the process of adhesion and spreading ARF re-localizes to sites of active actin polymerization and to focal adhesion points where it interacts with the phosphorylated focal adhesion kinase. In line with its recruitment to focal adhesions, we observe that hampering ARF function in cancer cells leads to gross defects in cytoskeleton organization resulting in apoptosis through a mechanism dependent on the Death-Associated Protein Kinase. Our data uncover a novel function for p14ARF in protecting cells from anoikis that may reflect its role in anchorage independence, a hallmark of malignant tumor cells.
[Mh] Termos MeSH primário: Anoikis/fisiologia
Adesão Celular/fisiologia
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Adesões Focais/metabolismo
Proteína Supressora de Tumor p14ARF/metabolismo
[Mh] Termos MeSH secundário: Apoptose/fisiologia
Linhagem Celular Tumoral
Proliferação Celular/fisiologia
Sobrevivência Celular/fisiologia
Citoesqueleto/metabolismo
Citoesqueleto/fisiologia
Proteínas Quinases Associadas com Morte Celular/metabolismo
Adesões Focais/fisiologia
Células HeLa
Seres Humanos
Células MCF-7
Fosforilação/fisiologia
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p14ARF); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.104


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[PMID]:28421310
[Au] Autor:Strzelczyk JK; Golabek K; Cuber P; Krakowczyk L; Owczarek AJ; Fronczek M; Choreza P; Hudziec E; Ostrowska Z
[Ad] Endereço:Department of Medical and Molecular Biology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia in Katowice, Jordana 19 Str., 41-808, Zabrze, Poland. asia.strzelczyk@gmail.com.
[Ti] Título:Comparison of Selected Protein Levels in Tumour and Surgical Margin in a Group of Patients with Oral Cavity Cancer.
[So] Source:Biochem Genet;55(4):322-334, 2017 Aug.
[Is] ISSN:1573-4927
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oral cavity cancer belongs to head-and-neck squamous cell carcinoma group. The purpose of the study was to assess the levels of certain proteins in a tumour and surgical margin in a group of patients with oral cavity cancer. The levels of DAPK1, MGMT, CDH1, SFRP1, SFRP2, RORA, TIMP3, p16, APC and RASSF1 proteins were measured by ELISA in tissue homogenates. The protein levels of DAPK1, MGMT, CDH1, SFRP2 and RASSF1 were significantly higher in tumour tissue than in the margin, contrary to TIMP3 which was lower in the tumour itself. DAPK1 level in the tumour was significantly higher in females than in males, the MGMT and p16 levels were lower in the tumours with lymph node metastasis (N1 + N2) than in N0 samples. The CDH1 expression was higher in a group with smoking habits, whereas TIMP3 was lower in this group. Changes in the levels of proteins in tumour and surgical margin may be either reflective of tumour occurrence and development, or they might be also responsible for the progress and reoccurrence of the disease. Levels of the studied proteins might be good prognostic factors; however, further studies are required.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/cirurgia
Metilação de DNA/genética
Neoplasias Bucais/cirurgia
Proteínas de Neoplasias/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Caderinas/biossíntese
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Proteínas Quinases Associadas com Morte Celular/biossíntese
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Metástase Linfática
Masculino
Meia-Idade
Boca/patologia
Boca/cirurgia
Neoplasias Bucais/genética
Neoplasias Bucais/patologia
Regiões Promotoras Genéticas
Inibidor Tecidual de Metaloproteinase-3/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Neoplasm Proteins); 0 (TIMP3 protein, human); 0 (Tissue Inhibitor of Metalloproteinase-3); EC 2.7.11.1 (DAPK1 protein, human); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1007/s10528-017-9799-4


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[PMID]:28391288
[Au] Autor:Jiang Y; Xu P; Yao D; Chen X; Dai H
[Ad] Endereço:Department of Hematology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China (mainland).
[Ti] Título:CD33, CD96 and Death Associated Protein Kinase (DAPK) Expression Are Associated with the Survival Rate and/or Response to the Chemotherapy in the Patients with Acute Myeloid Leukemia (AML).
[So] Source:Med Sci Monit;23:1725-1732, 2017 Apr 09.
[Is] ISSN:1643-3750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Leukemia stem cells (LSC) are involved in the incidence, drug resistance, and relapse of leukemia while LSC-related antigen CD33, CD96, and DAPK expression in AML and its prognosis is still unclear. This study explored LSC-related antigens expression in acute myeloid leukemia (AML) and its prognosis. MATERIAL AND METHODS A total of 156 cases of AML patients were enrolled in the experiment. The expression of CD33, CD96, and DAPK in CD34+CD38-CD123+ LSC were tested by flow cytometry. The survival curve was established using the Kaplan-Meier method. RESULTS Among different subtypes of AML, the positive rate of CD33 was M3> M5> M1> M2> M4; for CD96 it was M5> M4> M2> M3> M1; and for DAPK it was M3> M2> M5> M4> M1. After chemotherapy, the response rate in CD33 and CD96 high expression groups, and DAPK low expression group was significantly lower than the groups with CD33 low expression, CD96 low expression, and DAPK high expression. The median survival time in the CD33 high expression group was markedly lower than the CD33 low expression group (36.5 months). The CD96 high expression group exhibited obviously shorter median survival time than the CD96 low expression group. The DAPK high expression group exhibited longer median survival time than the DAPK low expression group. CONCLUSIONS CD33 and CD96 overexpression, and DAPK downregulation in the LSC of AML patients were associated with poor chemotherapy effect and prognosis, and higher recurrence rate.
[Mh] Termos MeSH primário: Células da Medula Óssea/metabolismo
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Antígenos CD/genética
Antígenos CD/metabolismo
Biomarcadores Farmacológicos
Células da Medula Óssea/imunologia
Proteínas Quinases Associadas com Morte Celular/genética
Proteínas Quinases Associadas com Morte Celular/metabolismo
Feminino
Citometria de Fluxo
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/imunologia
Masculino
Meia-Idade
Células-Tronco Neoplásicas/imunologia
Células-Tronco Neoplásicas/metabolismo
Prognóstico
Lectina 3 Semelhante a Ig de Ligação ao Ácido Siálico/genética
Lectina 3 Semelhante a Ig de Ligação ao Ácido Siálico/metabolismo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers, Pharmacological); 0 (CD33 protein, human); 0 (CD97 protein, human); 0 (Sialic Acid Binding Ig-like Lectin 3); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170410
[St] Status:MEDLINE


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[PMID]:28388658
[Au] Autor:Xie JY; Chen PC; Zhang JL; Gao ZS; Neves H; Zhang SD; Wen Q; Chen WD; Kwok HF; Lin Y
[Ad] Endereço:Department of Urology, The Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian Province, People's Republic of China.
[Ti] Título:The prognostic significance of DAPK1 in bladder cancer.
[So] Source:PLoS One;12(4):e0175290, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bladder cancer is one of the leading causes of cancer-related death in men, however, there was only limited effective treatment for invasive bladder cancer. DAPK1 has been shown to play important role in apoptosis and autophagy to suppress cancer progression. Previous results have shown that DAPK1 promoter was hypermethylated in the majority of bladder cancer specimens, however, the prognostic significance of DAPK1 in bladder cancer has yet to be demonstrated. In the present study, we found that DAPK1 expression was negatively associated with tumor stage and a low level expression of DAPK1 in bladder cancer specimens were associated with shorter survival in bladder cancer patients in 3 independent bladder cancer datasets (n = 462). Further investigation showed that FGFR3 knockdown resulted in downregulation of DAPK1 in bladder cancer cell line, suggesting that FGFR3 may be an upstream factor of DAPK1. Further analysis of the 3 independent bladder cancer datasets have identified ACOX1, UPK2, TRAK1, PLEKHG6 and MT1X genes had their expression significantly correlated with that of DAPK1. Knockdown of DAPK1 in bladder cancer T24 cells resulted in downregulation of ACOX1, UPK2 and TRAK1. Interestingly, TRAK1, by itself, was a favorable prognostic marker in the 3 independent bladder cancer datasets. Importantly, by using connectivity mapping with DAPK1-associated gene signature, we found that vemurafenib and trametinib could possibly reverse DAPK1-associated gene signature, suggesting that inhibition of Raf/MEK pathway may be a potential therapeutic approach for bladder cancer. Indeed, treatment of vemurafenib in T24 bladder cancer cells resulted in upregulation of DAPK1 confirming our connectivity mapping, while knockdown of DAPK1 resulted in reduced sensitivity towards inhibition of Braf signaling by vemurafenib. Together, our results suggest that DAPK1 is an important prognostic marker and therapeutic target for bladder cancer and have identified possible therapeutic agents for future testing in bladder cancer models with low DAPK1 expression.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Proteínas Quinases Associadas com Morte Celular/metabolismo
Neoplasias da Bexiga Urinária/patologia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Linhagem Celular Tumoral
Proteínas Quinases Associadas com Morte Celular/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Prognóstico
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptor Tipo 3 de Fator de Crescimento de Fibroblastos/genética
Receptor Tipo 3 de Fator de Crescimento de Fibroblastos/metabolismo
Neoplasias da Bexiga Urinária/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (RNA, Messenger); EC 2.7.10.1 (FGFR3 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 3); EC 2.7.11.1 (DAPK1 protein, human); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175290


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[PMID]:28378885
[Au] Autor:Wedge E; Hansen JW; Garde C; Asmar F; Tholstrup D; Kristensen SS; Munch-Petersen HD; Ralfkiaer E; Brown P; Grønbaek K; Kristensen LS
[Ad] Endereço:Department of Haematology, Rigshospitalet, Copenhagen, Denmark.
[Ti] Título:Global hypomethylation is an independent prognostic factor in diffuse large B cell lymphoma.
[So] Source:Am J Hematol;92(7):689-694, 2017 Jul.
[Is] ISSN:1096-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Global hypomethylation has been linked to disease progression in several cancers, but has not been reported for Diffuse Large B Cell Lymphoma (DLBCL). This study aimed to assess global methylation in DLBCL and describe its prognostic value. Mean LINE1 methylation, a validated surrogate measure for global methylation, was measured in DNA from 67 tumor biopsies. Additionally, cell-free circulating DNA (cfDNA) in plasma samples from 74 patients was tested to assess the feasibility of global hypomethylation as a biomarker in liquid biopsies. LINE1 methylation was assessed using a commercially available kit, based on pyrosequencing of PCR amplified bisulfite-treated DNA. Global hypomethylation was detected in a subset of cases and was associated with poor overall survival in both tumor biopsies (P = .001) and cfDNA (P = .009). It was the strongest risk factor in multivariate analysis in both biopsies (HR: 10.65, CI: 2.03-55.81, P = .005) and cfDNA (HR: 11.87, CI: 2.80-50.20, P = .001), outperforming conventional clinical risk factors. Finally, hierarchical cluster analyses were performed for the cfDNA samples using previously published gene-specific methylation data. This analysis shows that global hypomethylation co-occurs with other epigenetic abnormalities, including DAPK1 promoter hypermethylation. In conclusion, we have shown that global hypomethylation is strongly associated with poor survival in DLBCL both when present in tumor biopsy DNA and when detected in plasma cfDNA, and has potential for clinical application as a prognostic biomarker.
[Mh] Termos MeSH primário: Biomarcadores Tumorais
Metilação de DNA
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/mortalidade
[Mh] Termos MeSH secundário: Adulto
Idoso
Biópsia
Análise por Conglomerados
DNA de Neoplasias/sangue
DNA de Neoplasias/genética
Proteínas Quinases Associadas com Morte Celular/genética
Epigênese Genética
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Elementos Nucleotídeos Longos e Dispersos
Linfoma Difuso de Grandes Células B/diagnóstico
Linfoma Difuso de Grandes Células B/tratamento farmacológico
Masculino
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Regiões Promotoras Genéticas
Modelos de Riscos Proporcionais
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (DNA, Neoplasm); EC 2.7.11.1 (DAPK1 protein, human); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1002/ajh.24751



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