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  1 / 908 MEDLINE  
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[PMID]:27779297
[Au] Autor:Han KH; Kim MA; Park NH
[Ad] Endereço:Department of Obstetrics and Gynecology, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Republic of Korea.
[Ti] Título:Expression of aurora kinases: Predictor of tumor dissemination in uterine carcinosarcoma.
[So] Source:Histol Histopathol;32(7):717-724, 2017 Jul.
[Is] ISSN:1699-5848
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Uterine carcinosarcoma is a rare, aggressive, and biphasic tumor. It comprises carcinomatous and sarcomatous components, and mitosis-associated factors are thought to discriminate these two lesions. Aurora kinases are mitotic enzymes that are highly expressed in uterine malignancies. To identify the clinical significance of aurora kinase expression, we performed immunohistochemistry on tissue microarrays using cores selected from areas with typical carcinomatous and sarcomatous characteristics. A total of 24 samples were included, from patients at Seoul National University Hospital diagnosed with uterine carcinosarcoma, and who undergone a staging operation between 1997 and 2012. Patients' clinical and pathological data were analyzed, and expression patterns of aurora kinases were investigated. Aurora kinases A and B were dominantly expressed in the cytoplasm, and phospho-aurora kinases A and B were expressed in the nuclei. Phospho-aurora kinase A and aurora kinase B showed significantly higher expression in the carcinomatous component (P=0.012 and 0.008). High expression of phospho-aurora kinase A was associated with lymphatic metastasis such as positive pelvic lymph node and omental involvement (P=0.012 and 0.037). Overexpression of aurora kinase B was related to vascular invasion (P=0.011). High expression of both phospho-aurora kinase A and aurora kinase B was a prognostic factor for progression-free survival in uterine carcinosarcoma (P=0.049). In conclusion, expression of aurora kinases is associated with bidirectional tumor dissemination into the lymphatic and hematogenous pathways. In addition, high expression of phospho-aurora kinase A and aurora kinase B is a predictor of progression-free survival. Therefore, inhibitors of aurora kinases might be a prospective therapeutic options for uterine carcinosarcoma.
[Mh] Termos MeSH primário: Aurora Quinases/biossíntese
Carcinossarcoma/enzimologia
Carcinossarcoma/patologia
Neoplasias Uterinas/enzimologia
Neoplasias Uterinas/patologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Aurora Quinase A/metabolismo
Aurora Quinase B/metabolismo
Aurora Quinases/genética
Biomarcadores Tumorais
Intervalo Livre de Doença
Feminino
Regulação Enzimológica da Expressão Gênica/genética
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Menopausa
Meia-Idade
Metástase Neoplásica/patologia
Estadiamento de Neoplasias
Valor Preditivo dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.7.11.1 (AURKA protein, human); EC 2.7.11.1 (AURKB protein, human); EC 2.7.11.1 (Aurora Kinase A); EC 2.7.11.1 (Aurora Kinase B); EC 2.7.11.1 (Aurora Kinases)
[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:161026
[St] Status:MEDLINE
[do] DOI:10.14670/HH-11-834


  2 / 908 MEDLINE  
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[PMID]:29358147
[Au] Autor:Long L; Luo Y; Hou ZJ; Ma HJ; Long ZJ; Tu ZC; Huang LJ; Liu Q; Lu G
[Ad] Endereço:Institute of Medicinal Chemistry, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, PR China.
[Ti] Título:Synthesis and biological evaluation of aurora kinases inhibitors based on N-trisubstituted pyrimidine scaffold.
[So] Source:Eur J Med Chem;145:805-812, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The inhibition of the members of aurora kinase family using ATP-competitive small molecules is an effective method for anticancer therapeutics. Based on our previous work, we synthesized 12 new N-trisubstituted pyrimidine derivatives and evaluated their biological activities and stabilities. Among them, compound 11j showed the best inhibition against aurora A kinase (IC = 7.1 nM), human leukemia cell line U937 (IC = 12.2 nM) and the growth of U937 xenograft tumors in vivo. By the flow cytometry and immunofluorescence analysis of U937, we found that compound 11j can induced polyploidy formation including (4N, 8N and 16N) and induce defects in both chromosome alignment and spindle formation. Furthermore, compound 11j exhibited good chemical, physical, and thermal stabilities. All these results suggested that 11j is a promising lead compound for further development of anticancer drugs.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Antineoplásicos/química
Aurora Quinase A/antagonistas & inibidores
Aurora Quinase A/metabolismo
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Camundongos
Camundongos Nus
Estrutura Molecular
Neoplasias Experimentais/tratamento farmacológico
Neoplasias Experimentais/patologia
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Pirimidinas/síntese química
Pirimidinas/química
Relação Estrutura-Atividade
Células U937
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); EC 2.7.11.1 (Aurora Kinase A)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE


  3 / 908 MEDLINE  
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[PMID]:29260599
[Au] Autor:Liewer S; Huddleston A
[Ad] Endereço:a Department of Pharmacy , Nebraska Medicine , Omaha , NE , USA.
[Ti] Título:Alisertib: a review of pharmacokinetics, efficacy and toxicity in patients with hematologic malignancies and solid tumors.
[So] Source:Expert Opin Investig Drugs;27(1):105-112, 2018 Jan.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Aurora kinases are essential mediators in cell mitosis. Amplification of these kinases can lead to the development of malignancy and may be associated with inferior survival. Alisertib is an oral aurora kinase inhibitor which has been shown to induce cell-cycle arrest and apoptosis in preclinical studies. It is currently under investigation for a wide variety of malignancies including hematologic (specifically Non-Hodgkin's lymphoma) and solid tumors. Areas covered: A PubMed search was performed to identify clinical studies reporting outcomes with alisertib. Promising results are notable in patients with peripheral T cell lymphoma in particular, forming the basis for the first phase 3 randomized trial of alisertib. Although it did show encouraging response rates, it failed to demonstrate superiority over the comparator arm at an interim analysis, halting further enrollment. Expert opinion: Despite disappointing early results, alisertib remains under investigation in a number of cancer types both as monotherapy and in combination with traditional cytotoxic chemotherapy, with encouraging results. Most common toxicities in early trials include myelosuppression alopecia, mucositis and fatigue. The relatively manageable toxicity profile of alisertib along with ease of dosing may allow it to be combined with other oral agents or traditional chemotherapy across a wide variety of malignancy types.
[Mh] Termos MeSH primário: Azepinas/administração & dosagem
Linfoma não Hodgkin/tratamento farmacológico
Neoplasias/tratamento farmacológico
Pirimidinas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Antineoplásicos/efeitos adversos
Antineoplásicos/farmacocinética
Apoptose/efeitos dos fármacos
Aurora Quinase A/antagonistas & inibidores
Azepinas/efeitos adversos
Azepinas/farmacocinética
Seres Humanos
Linfoma não Hodgkin/patologia
Neoplasias/patologia
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/efeitos adversos
Inibidores de Proteínas Quinases/farmacocinética
Pirimidinas/efeitos adversos
Pirimidinas/farmacocinética
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Azepines); 0 (MLN 8237); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); EC 2.7.11.1 (Aurora Kinase A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2018.1417382


  4 / 908 MEDLINE  
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[PMID]:28470610
[Au] Autor:Dodson CA
[Ad] Endereço:Molecular Medicine, National Heart & Lung Institute, Imperial College London, SAF Building, Room 364, South Kensington Campus, London, SW7 2AZ, UK. c.dodson@imperial.ac.uk.
[Ti] Título:Production of Protein Kinases in E. coli.
[So] Source:Methods Mol Biol;1586:251-264, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recombinant protein expression is widely used to generate milligram quantities of protein kinases for crystallographic, enzymatic, or other biophysical assays in vitro. Expression in E. coli is fast, cheap, and reliable. Here I present a detailed protocol for the production of human Aurora-A kinase. I begin with transformation of a suitable plasmid into an expression strain of E. coli, followed by growth and harvesting of bacterial cell cultures. Finally, I describe the purification of Aurora-A to homogeneity using immobilized metal affinity and size exclusion chromatographies.
[Mh] Termos MeSH primário: Aurora Quinase A/genética
Clonagem Molecular/métodos
Escherichia coli/genética
[Mh] Termos MeSH secundário: Aurora Quinase A/isolamento & purificação
Cromatografia de Afinidade/métodos
Cromatografia em Gel/métodos
Seres Humanos
Plasmídeos/genética
Proteínas Recombinantes/genética
Proteínas Recombinantes/isolamento & purificação
Transformação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Recombinant Proteins); EC 2.7.11.1 (AURKA protein, human); EC 2.7.11.1 (Aurora Kinase A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6887-9_16


  5 / 908 MEDLINE  
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[PMID]:29202611
[Au] Autor:Lykkesfeldt AE; Iversen BR; Jensen MB; Ejlertsen B; Giobbie-Hurder A; Reiter BE; Kirkegaard T; Rasmussen BB
[Ad] Endereço:a Unit of Cell Death and Metabolism , Danish Cancer Society Research Center , Copenhagen , Denmark.
[Ti] Título:Aurora kinase A as a possible marker for endocrine resistance in early estrogen receptor positive breast cancer.
[So] Source:Acta Oncol;57(1):67-73, 2018 Jan.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell culture studies have disclosed that the mitotic Aurora kinase A is causally involved in both tamoxifen and aromatase inhibitor resistant cell growth and thus may be a potential new marker for endocrine resistance in the clinical setting. MATERIAL AND METHODS: Archival tumor tissue was available from 1323 Danish patients with estrogen receptor (ER) positive primary breast cancer, who participated in the Breast International Group (BIG) 1-98 trial, comparing treatment with tamoxifen and letrozole and both in a sequence. The expression of Aurora A was determined by immunohistochemistry in 980 tumors and semi quantitively scored into three groups; negative/weak, moderate and high. The Aurora A expression levels were compared to other clinico-pathological parameters and outcome, defined as disease-free survival (DFS) and overall survival (OS). RESULTS: High expression of Aurora A was found in 26.9% of patients and moderate in 57.0%. High expression was significantly associated with high malignancy grade and HER2 amplification. High Aurora A expression was significantly more frequent in ductal compared to lobular carcinomas. We found no significant association between Aurora A expression and DFS or OS and no evidence of interaction between Aurora A expression and benefits from tamoxifen versus letrozole. CONCLUSIONS: Aurora A expression in breast tumors was associated with high malignancy grade III and with HER2 amplification. A trend as a prognostic factor for OS was found in patients with high Aurora A expression. No predictive property was observed in this study with early breast cancer.
[Mh] Termos MeSH primário: Aurora Quinase A/metabolismo
Neoplasias da Mama/metabolismo
Neoplasias da Mama/mortalidade
Resistência a Medicamentos Antineoplásicos
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos Hormonais/uso terapêutico
Inibidores da Aromatase/uso terapêutico
Biomarcadores/metabolismo
Neoplasias da Mama/patologia
Neoplasias da Mama/terapia
Carcinoma Ductal de Mama/metabolismo
Carcinoma Ductal de Mama/mortalidade
Carcinoma Ductal de Mama/patologia
Carcinoma Ductal de Mama/terapia
Carcinoma Lobular/metabolismo
Carcinoma Lobular/mortalidade
Carcinoma Lobular/patologia
Carcinoma Lobular/terapia
Dinamarca/epidemiologia
Intervalo Livre de Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Nitrilos/uso terapêutico
Prognóstico
Receptor ErbB-2/metabolismo
Tamoxifeno/uso terapêutico
Triazóis/uso terapêutico
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Aromatase Inhibitors); 0 (Biomarkers); 0 (Nitriles); 0 (Receptors, Estrogen); 0 (Triazoles); 094ZI81Y45 (Tamoxifen); 7LKK855W8I (letrozole); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.11.1 (Aurora Kinase A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1080/0284186X.2017.1404126


  6 / 908 MEDLINE  
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[PMID]:29115879
[Au] Autor:Kurup S; McAllister B; Liskova P; Mistry T; Fanizza A; Stanford D; Slawska J; Keller U; Hoellein A
[Ad] Endereço:a College of Pharmacy , Roosevelt University , Schaumburg , IL , USA.
[Ti] Título:Design, synthesis and biological activity of N -phenylsubstituted-7H-pyrrolo[2,3-d]pyrimidin-4-amines as dual inhibitors of aurora kinase A and epidermal growth factor receptor kinase.
[So] Source:J Enzyme Inhib Med Chem;33(1):74-84, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Simultaneous inhibition of multiple kinases has been suggested to provide synergistic effects on inhibition of tumour growth and resistance. This study describes the design, synthesis and evaluation of 18 compounds incorporating a pyrrolo[2,3-d]pyrimidine scaffold for dual inhibition of epidermal growth factor receptor kinase (EGFR) and aurora kinase A (AURKA). Compounds 1-18 of this study demonstrate nanomolar inhibition of EGFR and micromolar inhibition of AURKA. Compounds 1-18 allow for a structure-activity relationships (SAR) analysis of the 4-anilino moiety for dual EGFR and AURKA inhibition. Compound 6, a 4-methoxyphenylpyrrolo[2,3-d]pyrimidin-4-amine, demonstrates single-digit micromolar inhibition of both AURKA and EGFR and provides evidence of a single molecule with dual activity against EGFR and AURKA. Compound 2, the most potent inhibitor of EGFR and AURKA from this series, has been further evaluated in four different squamous cell head and neck cancer cell lines for downstream effects resulting from AURKA and EGFR inhibition.
[Mh] Termos MeSH primário: Aurora Quinase A/antagonistas & inibidores
Desenho de Drogas
Modelos Moleculares
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Pirróis/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Aurora Quinase A/metabolismo
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Estrutura Molecular
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Pirimidinas/síntese química
Pirimidinas/química
Pirróis/síntese química
Pirróis/química
Receptor do Fator de Crescimento Epidérmico/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (N4-(4-methoxyphenyl)-7H-pyrrolo(2,3-d)pyrimidine-4-amine); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Pyrroles); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (AURKA protein, human); EC 2.7.11.1 (Aurora Kinase A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171109
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1376666


  7 / 908 MEDLINE  
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[PMID]:28884479
[Au] Autor:Yang TY; Teng CJ; Lin TC; Chen KC; Hsu SL; Wu CC
[Ad] Endereço:Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, 407, Taiwan, Republic of China.
[Ti] Título:Transcriptional repression of Aurora-A gene by wild-type p53 through directly binding to its promoter with histone deacetylase 1 and mSin3a.
[So] Source:Int J Cancer;142(1):92-108, 2018 Jan 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we firstly showed that p53 transcriptionally represses Aurora-A gene expression through directly binding to its promoter. DNA affinity precipitation assay and chromatin immunoprecipitation assay indicated that p53 physically bound to the Aurora-A promoter. Moreover, the in vitro and in vivo assays showed that p53 directly bound to the Aurora-A promoter together with histone deacetylase 1 (HDAC1) and mSin3a as corepressors. Furthermore, we identified that the nucleotides -360 to -354 (CCTGCCC), upstream of the Aurora-A transcriptional start site, was responsible for the p53-mediated repression. Mutation within this site disrupted its interaction with p53, mSin3a and HDAC1, as well as attenuated the repressive effect of p53 on Aurora-A promoter activity. Treatment with trichostatin A (TSA), a HDAC1 inhibitor, disrupted the interaction of p53-HDAC1-mSin3a complex with the nucleotides -365∼-345 region, and enhanced the Aurora-A promoter activity and gene expression. Additionally, knockdown of p53 or mSin3a also drastically blocked the formation of p53-HDAC1-mSin3a repressive complex onto this promoter region and elevated the Aurora-A promoter activity and gene expression. Moreover, the p53-HDAC1-mSin3a repressive complex also involved in the inhibition of Aurora-A gene expression upon cisplatin treatment. Finally, the clinical investigation showed that Aurora-A and p53 exhibited an inverse correlation in both the expression level and prognostic status, and the low p53/high Aurora-A showed the poorest prognosis of NSCLC patients. Our findings showed novel regulatory mechanisms of p53 in regulating Aurora-A gene expression in NSCLC cells.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Aurora Quinase A/biossíntese
Regulação Neoplásica da Expressão Gênica/genética
Neoplasias Pulmonares/genética
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Aurora Quinase A/genética
Linhagem Celular Tumoral
Histona Desacetilase 1/genética
Histona Desacetilase 1/metabolismo
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/mortalidade
Regiões Promotoras Genéticas/genética
Transcrição Genética/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53); EC 2.7.11.1 (AURKA protein, human); EC 2.7.11.1 (Aurora Kinase A); EC 3.5.1.98 (HDAC1 protein, human); EC 3.5.1.98 (Histone Deacetylase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31035


  8 / 908 MEDLINE  
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[PMID]:28935709
[Au] Autor:Wang H; Choe MH; Lee IW; Namgoong S; Kim JS; Kim NH; Oh JS
[Ad] Endereço:Department of Animal Sciences, Chungbuk National University, Cheongju 28644, Korea.
[Ti] Título:CIP2A acts as a scaffold for CEP192-mediated microtubule organizing center assembly by recruiting Plk1 and aurora A during meiotic maturation.
[So] Source:Development;144(20):3829-3839, 2017 10 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In somatic cells spindle microtubules are nucleated from centrosomes that act as major microtubule organizing centers (MTOCs), whereas oocytes form meiotic spindles by assembling multiple acentriolar MTOCs without canonical centrosomes. Aurora A and Plk1 are required for these events, but the underlying mechanisms remain largely unknown. Here we show that CIP2A regulates MTOC organization by recruiting aurora A and Plk1 at spindle poles during meiotic maturation. CIP2A colocalized with pericentrin at spindle poles with a few distinct cytoplasmic foci. Although CIP2A has been identified as an endogenous inhibitor of protein phosphatase 2A (PP2A), overexpression of CIP2A had no effect on meiotic maturation. Depletion of CIP2A perturbed normal spindle organization and chromosome alignment by impairing MTOC organization. Importantly, CIP2A was reciprocally associated with CEP192, promoting recruitment of aurora A and Plk1 at MTOCs. CIP2A was phosphorylated by Plk1 at S904, which targets CIP2A to MTOCs and facilitates MTOC organization with CEP192. Our results suggest that CIP2A acts as a scaffold for CEP192-mediated MTOC assembly by recruiting Plk1 and aurora A during meiotic maturation in mouse oocytes.
[Mh] Termos MeSH primário: Aurora Quinase A/genética
Autoantígenos/fisiologia
Proteínas de Ciclo Celular/fisiologia
Proteínas Cromossômicas não Histona/fisiologia
Proteínas de Membrana/fisiologia
Centro Organizador dos Microtúbulos
Proteínas Serina-Treonina Quinases/fisiologia
Proteínas Proto-Oncogênicas/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos/metabolismo
Autoantígenos/genética
Proteínas de Ciclo Celular/genética
Centrossomo/metabolismo
Proteínas Cromossômicas não Histona/genética
Segregação de Cromossomos
Citoplasma/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Meiose
Proteínas de Membrana/genética
Camundongos
Microtúbulos/metabolismo
Oócitos/metabolismo
Ovário/metabolismo
Fosforilação
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
RNA Interferente Pequeno/metabolismo
Fuso Acromático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Autoantigens); 0 (CEP192 protein, mouse); 0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (KIAA1524 protein, mouse); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 0 (RNA, Small Interfering); 0 (pericentrin); EC 2.7.11.1 (Aurka protein, mouse); EC 2.7.11.1 (Aurora Kinase A); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1242/dev.158584


  9 / 908 MEDLINE  
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[PMID]:28906374
[Au] Autor:Golmohammadi R; Namazi MJ; Going JJ; Derakhshan MH
[Ad] Endereço:aDepartment of Anatomy, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran bDepartment of Microbiology and Immunology, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran cAcademic Unit of Medical Genetics and Pathology, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
[Ti] Título:A single nucleotide polymorphism in codon F31I and V57I of the AURKA gene in invasive ductal breast carcinoma in Middle East.
[So] Source:Medicine (Baltimore);96(37):e7933, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although few studies have suggested a carcinogenic role for polymorphism of F31I and V57I codons of AURKA gene in invasive ductal carcinoma, contradictory results from different populations mandates regional investigations. We aimed to determine polymorphisms of F31I and V57I codons of AURKA gene and their association with cancer prognosis in patients compared with controls in an eastern population of Iran.A case-control study was conducted on specimens from 100 patients and 100 age- and gender-matched controls. DNA was extracted and the codons F31I and V57I were amplified. The different genotypes were analyzed by PCR-RFLP and electrophoresis.In codon F31I, the frequency of Phe/Ile was 70% and 82% in patients and healthy controls respectively, whereas (Ile/Ile) was 30% in patients and 18% in healthy (P = .047). Analyzing V57I genotypes showed a higher homozygote Val/Val genotype in patients compared with controls (76% vs 68%), whereas the frequency of heterozygous Val/Ile genotype was lower in patients (17%) than controls (30%), yielding a marginal association between breast cancer and Val/Val genotype (P = .048). No association was observed between SNPs of either F31I or V57I genotypes and histological grades. However, there was a significant association between tumor stages and F31I genotype (P for trend = .003).This is the first report of F31I and V57I polymorphisms in AURKA gene in breast cancer in Iran. Determination of allelic polymorphism of those codons will help to understand background genetic predisposition and could have prognostic value in management of breast cancer in the target population.
[Mh] Termos MeSH primário: Aurora Quinase A/genética
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/genética
Carcinoma Ductal de Mama/patologia
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/mortalidade
Carcinoma Ductal de Mama/mortalidade
Estudos de Casos e Controles
Códon
Feminino
Seres Humanos
Irã (Geográfico)
Meia-Idade
Invasividade Neoplásica
Prognóstico
Taxa de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon); EC 2.7.11.1 (Aurora Kinase A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007933


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[PMID]:28720575
[Au] Autor:Sampson J; O'Regan L; Dyer MJS; Bayliss R; Fry AM
[Ad] Endereço:Department of Molecular and Cell Biology, University of Leicester, Leicester, United Kingdom.
[Ti] Título:Hsp72 and Nek6 Cooperate to Cluster Amplified Centrosomes in Cancer Cells.
[So] Source:Cancer Res;77(18):4785-4796, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cells frequently possess extra amplified centrosomes clustered into two poles whose pseudo-bipolar spindles exhibit reduced fidelity of chromosome segregation and promote genetic instability. Inhibition of centrosome clustering triggers multipolar spindle formation and mitotic catastrophe, offering an attractive therapeutic approach to selectively kill cells with amplified centrosomes. However, mechanisms of centrosome clustering remain poorly understood. Here, we identify a new pathway that acts through NIMA-related kinase 6 (Nek6) and Hsp72 to promote centrosome clustering. Nek6, as well as its upstream activators polo-like kinase 1 and Aurora-A, targeted Hsp72 to the poles of cells with amplified centrosomes. Unlike some centrosome declustering agents, blocking Hsp72 or Nek6 function did not induce formation of acentrosomal poles, meaning that multipolar spindles were observable only in cells with amplified centrosomes. Inhibition of Hsp72 in acute lymphoblastic leukemia cells resulted in increased multipolar spindle frequency that correlated with centrosome amplification, while loss of Hsp72 or Nek6 function in noncancer-derived cells disturbs neither spindle formation nor mitotic progression. Hence, the Nek6-Hsp72 module represents a novel actionable pathway for selective targeting of cancer cells with amplified centrosomes. .
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Centrossomo/patologia
Proteínas de Choque Térmico HSP72/metabolismo
Neuroblastoma/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Aurora Quinase A/genética
Aurora Quinase A/metabolismo
Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Proliferação Celular
Centrossomo/metabolismo
Feminino
Proteínas de Choque Térmico HSP72/genética
Seres Humanos
Camundongos
Mitose/fisiologia
Quinases Relacionadas a NIMA/genética
Quinases Relacionadas a NIMA/metabolismo
Neuroblastoma/genética
Neuroblastoma/metabolismo
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Fuso Acromático/metabolismo
Fuso Acromático/patologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (HSP72 Heat-Shock Proteins); 0 (Proto-Oncogene Proteins); EC 2.7.11.1 (Aurora Kinase A); EC 2.7.11.1 (NEK6 protein, human); EC 2.7.11.1 (NIMA-Related Kinases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-3233



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