Base de dados : MEDLINE
Pesquisa : D02.092.080 [Categoria DeCS]
Referências encontradas : 3709 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 371 ir para página                         

  1 / 3709 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29272749
[Au] Autor:Liessi N; Cichero E; Pesce E; Arkel M; Salis A; Tomati V; Paccagnella M; Damonte G; Tasso B; Galietta LJV; Pedemonte N; Fossa P; Millo E
[Ad] Endereço:Department of Experimental Medicine, Section of Biochemistry, University of Genoa, Viale Benedetto XV 1, 16132 Genoa, Italy; Center of Excellence for Biomedical Research (CEBR), University of Genoa, Viale Benedetto XV 9, 16132 Genoa, Italy.
[Ti] Título:Synthesis and biological evaluation of novel thiazole- VX-809 hybrid derivatives as F508del correctors by QSAR-based filtering tools.
[So] Source:Eur J Med Chem;144:179-200, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The most common CF mutation, F508del, impairs the processing and gating of CFTR protein. This deletion results in the improper folding of the protein and its degradation before it reaches the plasma membrane of epithelial cells. Present correctors, like VX809 only induce a partial rescue of the mutant protein. Our previous studies reported a class of compounds, called aminoarylthiazoles (AATs), featuring an interesting activity as correctors. Some of them show additive effect with VX809 indicating a different mechanism of action. In an attempt to construct more interesting molecules, it was thought to generate chemically hybrid compounds, blending a portion of VX809 merged to the thiazole scaffold. This approach was guided by the development of QSAR analyses, which were performed based on the F508del correctors so far disclosed in the literature. This strategy was aimed at exploring the key requirements turning in the corrector ability of the collected derivatives and allowed us to derive a predictive model guiding for the synthesis of novel hybrids as promising correctors. The new molecules were tested in functional and biochemical assays on bronchial CFBE41o-cells expressing F508del-CFTR showing a promising corrector activity.
[Mh] Termos MeSH primário: Aminopiridinas/química
Aminopiridinas/farmacologia
Benzodioxóis/química
Benzodioxóis/farmacologia
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Mutação/efeitos dos fármacos
Tiazóis/química
Tiazóis/farmacologia
[Mh] Termos MeSH secundário: Aminopiridinas/síntese química
Benzodioxóis/síntese química
Linhagem Celular
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Seres Humanos
Relação Quantitativa Estrutura-Atividade
Tiazóis/síntese química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminopyridines); 0 (Benzodioxoles); 0 (Thiazoles); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); EGP8L81APK (lumacaftor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE


  2 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29480865
[Au] Autor:Jin J; Zheng C; Wu S
[Ad] Endereço:Department of Hematology, Wenzhou Central Hospital, Theorem Clinical College, Wenzhou Medical University, Wenzhou, P.R. China.
[Ti] Título:Therapeutic effect of chidamide on relapsed refractory angioimmunoblastic T-cell lymphoma: A case report and literature review.
[So] Source:Medicine (Baltimore);97(2):e9611, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Angioimmunoblastic T-cell lymphoma (AITL) is a kind of rare peripheral T cell lymphoma, which usually has acute onset at old age. MATERIALS AND METHODS: Here we report a case of relapsed refractory AITL, which has achieved obvious curative effect after treatment with chidamide. RESULTS: Initially, the patient received 7 courses of treatment with recombinant human endostatin (endostar)+CHOP. The patient achieved complete remission, but suffered from recurrence later. After changing chemotherapy regimens, the outcome was still not satisfactory, and the patient developed systemic skin infiltration and rashes. After 2 courses of chemotherapy with chidamide (30 mg) twice a week + intravenous injections with cyclophosphamide (0.1 g) twice every other day + thalidomide (50 mg) every night, the patient began with the oral intake of chidamide, and the therapeutic effect was satisfactory, with diminishing systemic rashes and shrunken lymph nodes. DISCUSSION AND CONCLUSIONS: Chidamide has good therapeutic effect in the treatment of AITL, which provides a novel therapeutic strategy for relapsed refractory AITL. However, more cases are still needed to further validate its efficacy.
[Mh] Termos MeSH primário: Aminopiridinas/uso terapêutico
Antineoplásicos/uso terapêutico
Benzamidas/uso terapêutico
Linfoma de Células T Periférico/tratamento farmacológico
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica
Feminino
Seres Humanos
Linfoma de Células T Periférico/diagnóstico por imagem
Linfoma de Células T Periférico/patologia
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminopyridines); 0 (Antineoplastic Agents); 0 (Benzamides); 87CIC980Y0 (N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009611


  3 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29443750
[Au] Autor:Liu DY; Wang ZG; Gao Y; Zhang HM; Zhang YX; Wang XJ; Peng D
[Ad] Endereço:Department of Respiratory Medicine, The People's Hospital of Yan'an, Yan'an.
[Ti] Título:Effect and safety of roflumilast for chronic obstructive pulmonary disease in Chinese patients.
[So] Source:Medicine (Baltimore);97(7):e9864, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This trial aimed to evaluate the efficacy and safety of roflumilast for treating Chinese patients with chronic obstructive pulmonary disease (COPD). METHODS: A total of 120 patients with COPD were recruited and were randomly divided into 2 groups (an intervention group and a placebo group) at a 1:1 ratio. Patients received either roflumilast or placebo 500 µg once daily for a total of 12 months. The primary outcome was lung function, measured by the change from baseline of forced expiratory volume in 1 second (FEV1), FVC = forced vital capacity (FVC), and FEF25-75%. The secondary outcome measurements included the quality of life, measured with the St. George's Respiratory Questionnaire (SGRQ). All outcomes were measured at the end of 12-month treatment and 3-month follow-up after the treatment. In addition, adverse events (AEs) were also recorded during the treatment period. RESULTS: FEV1, FVC, FEF25-75%, and SGRQ were significantly better in the intervention group than those in the placebo group at the end of 12-month treatment and 3-month follow up after treatment. Moreover, AEs were much higher with roflumilast than placebo in this study. CONCLUSIONS: The findings suggest that roflumilast has promising effect to improve lung function in Chinese population with COPD.
[Mh] Termos MeSH primário: Aminopiridinas
Benzamidas
Doença Pulmonar Obstrutiva Crônica
Qualidade de Vida
[Mh] Termos MeSH secundário: Idoso
Aminopiridinas/administração & dosagem
Aminopiridinas/efeitos adversos
Grupo com Ancestrais do Continente Asiático
Benzamidas/administração & dosagem
Benzamidas/efeitos adversos
Ciclopropanos/administração & dosagem
Ciclopropanos/efeitos adversos
Método Duplo-Cego
Monitoramento de Medicamentos
Feminino
Seres Humanos
Masculino
Meia-Idade
Avaliação de Processos e Resultados (Cuidados de Saúde)
Inibidores da Fosfodiesterase 4/administração & dosagem
Inibidores da Fosfodiesterase 4/efeitos adversos
Doença Pulmonar Obstrutiva Crônica/diagnóstico
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
Doença Pulmonar Obstrutiva Crônica/etnologia
Doença Pulmonar Obstrutiva Crônica/psicologia
Testes de Função Respiratória/métodos
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Aminopyridines); 0 (Benzamides); 0 (Cyclopropanes); 0 (Phosphodiesterase 4 Inhibitors); 0P6C6ZOP5U (Roflumilast)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009864


  4 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28467931
[Au] Autor:Cokorinos EC; Delmore J; Reyes AR; Albuquerque B; Kjøbsted R; Jørgensen NO; Tran JL; Jatkar A; Cialdea K; Esquejo RM; Meissen J; Calabrese MF; Cordes J; Moccia R; Tess D; Salatto CT; Coskran TM; Opsahl AC; Flynn D; Blatnik M; Li W; Kindt E; Foretz M; Viollet B; Ward J; Kurumbail RG; Kalgutkar AS; Wojtaszewski JFP; Cameron KO; Miller RA
[Ad] Endereço:Cardiovascular, Metabolic, and Endocrine Diseases Research Unit, Pfizer Inc., Cambridge, MA 02139, USA.
[Ti] Título:Activation of Skeletal Muscle AMPK Promotes Glucose Disposal and Glucose Lowering in Non-human Primates and Mice.
[So] Source:Cell Metab;25(5):1147-1159.e10, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The AMP-activated protein kinase (AMPK) is a potential therapeutic target for metabolic diseases based on its reported actions in the liver and skeletal muscle. We evaluated two distinct direct activators of AMPK: a non-selective activator of all AMPK complexes, PF-739, and an activator selective for AMPK ß1-containing complexes, PF-249. In cells and animals, both compounds were effective at activating AMPK in hepatocytes, but only PF-739 was capable of activating AMPK in skeletal muscle. In diabetic mice, PF-739, but not PF-249, caused a rapid lowering of plasma glucose levels that was diminished in the absence of skeletal muscle, but not liver, AMPK heterotrimers and was the result of an increase in systemic glucose disposal with no impact on hepatic glucose production. Studies of PF-739 in cynomolgus monkeys confirmed translation of the glucose lowering and established activation of AMPK in skeletal muscle as a potential therapeutic approach to treat diabetic patients.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Aminopiridinas/farmacologia
Ativadores de Enzimas/farmacologia
Glucose/metabolismo
Hipoglicemiantes/farmacologia
Indóis/farmacologia
[Mh] Termos MeSH secundário: Aminopiridinas/uso terapêutico
Animais
Glicemia/metabolismo
Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Experimental/metabolismo
Ativação Enzimática/efeitos dos fármacos
Ativadores de Enzimas/uso terapêutico
Feminino
Hipoglicemiantes/uso terapêutico
Indóis/uso terapêutico
Fígado/efeitos dos fármacos
Fígado/metabolismo
Macaca fascicularis
Masculino
Camundongos Endogâmicos C57BL
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminopyridines); 0 (Blood Glucose); 0 (Enzyme Activators); 0 (Hypoglycemic Agents); 0 (Indoles); 0 (PF-249); EC 2.7.11.31 (AMP-Activated Protein Kinases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  5 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28459323
[Au] Autor:Ramsey BW; Welsh MJ
[Ad] Endereço:1 Department of Pediatrics University of Washington School of Medicine Seattle, Washington.
[Ti] Título:AJRCCM: 100-Year Anniversary. Progress along the Pathway of Discovery Leading to Treatment and Cure of Cystic Fibrosis.
[So] Source:Am J Respir Crit Care Med;195(9):1092-1099, 2017 05 01.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Aminofenóis/uso terapêutico
Aminopiridinas/uso terapêutico
Antibacterianos/uso terapêutico
Benzodioxóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Fibrose Cística/tratamento farmacológico
Publicações Periódicas como Assunto/história
Pneumologia/história
Quinolonas/uso terapêutico
[Mh] Termos MeSH secundário: Aniversários e Eventos Especiais
Fibrose Cística/genética
Fibrose Cística/história
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Combinação de Medicamentos
Terapia de Reposição de Enzimas
História do Século XX
História do Século XXI
Mutação
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Anti-Bacterial Agents); 0 (Benzodioxoles); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Drug Combinations); 0 (Quinolones); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201702-0266ED


  6 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29241892
[Au] Autor:Dilokthornsakul P; Patidar M; Campbell JD
[Ad] Endereço:Center of Pharmaceutical Outcomes Research, Department of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Naresuan University, Phitsanulok, Thailand. Electronic address: piyamethd@nu.ac.th.
[Ti] Título:Forecasting the Long-Term Clinical and Economic Outcomes of Lumacaftor/Ivacaftor in Cystic Fibrosis Patients with Homozygous phe508del Mutation.
[So] Source:Value Health;20(10):1329-1335, 2017 12.
[Is] ISSN:1524-4733
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To forecast lifetime outcomes and cost of lumacaftor/ivacaftor combination therapy in patients with cystic fibrosis (CF) with homozygous phe508del mutation from the US payer perspective. METHODS: A lifetime Markov model was developed from a US payer perspective. The model included five health states: 1) mild lung disease (percent predicted forced expiratory volume in 1 second [FEV ] >70%), 2) moderate lung disease (40% ≤ FEV ≤ 70%), 3) severe lung disease (FEV < 40%), 4) lung transplantation, and 5) death. All inputs were derived from published literature. We estimated lumacaftor/ivacaftor's improvement in outcomes compared with a non-CF referent population as well as CF-specific mortality estimates. RESULTS: Lumacaftor/ivacaftor was associated with additional 2.91 life-years (95% credible interval 2.55-3.56) and additional 2.42 quality-adjusted life-years (QALYs) (95% credible interval 2.10-2.98). Lumacaftor/ivacaftor was associated with improvements in survival and QALYs equivalent to 27.6% and 20.7%, respectively, for the survival and QALY gaps between CF usual care and their non-CF peers. The incremental lifetime cost was $2,632,249. CONCLUSIONS: Lumacaftor/ivacaftor increased life-years and QALYs in CF patients with the homozygous phe508del mutation and moved morbidity and mortality closer to that of their non-CF peers but it came with higher cost.
[Mh] Termos MeSH primário: Aminofenóis/administração & dosagem
Aminopiridinas/administração & dosagem
Benzodioxóis/administração & dosagem
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Fibrose Cística/tratamento farmacológico
Anos de Vida Ajustados por Qualidade de Vida
Quinolonas/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Aminofenóis/economia
Aminopiridinas/economia
Benzodioxóis/economia
Fibrose Cística/genética
Fibrose Cística/fisiopatologia
Combinação de Medicamentos
Volume Expiratório Forçado
Homozigoto
Seres Humanos
Cadeias de Markov
Mutação
Quinolonas/economia
Índice de Gravidade de Doença
Resultado do Tratamento
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (Drug Combinations); 0 (Quinolones); 0 (cystic fibrosis transmembrane conductance regulator delta F508); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  7 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28461409
[Au] Autor:Thomas D; Majeti R
[Ad] Endereço:Division of Hematology, Department of Medicine, Cancer Institute, and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California.
[Ti] Título:Optimizing Next-Generation AML Therapy: Activity of Mutant IDH2 Inhibitor AG-221 in Preclinical Models.
[So] Source:Cancer Discov;7(5):459-461, 2017 05.
[Is] ISSN:2159-8290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo: AG-221 or enasidenib is a first-in-class selective inhibitor of mutated isocitrate dehydrogenase 2 (IDH2) with early demonstrated clinical efficacy in acute myeloid leukemia as a single agent, yet with persistence of mutant clones. Two articles in this issue of provide further insight into the biological activity of AG-221 in promoting differentiation of -mutant cells and reversing aberrant DNA methylation over time, and demonstrating preclinical activity in combination with a targeted FLT3 kinase inhibitor to eliminate -mutant clones. .
[Mh] Termos MeSH primário: Isocitrato Desidrogenase/antagonistas & inibidores
Mutação
[Mh] Termos MeSH secundário: Aminopiridinas
Seres Humanos
Leucemia Mieloide Aguda/genética
Triazinas
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (AG-221); 0 (Aminopyridines); 0 (Triazines); EC 1.1.1.41 (Isocitrate Dehydrogenase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1158/2159-8290.CD-17-0270


  8 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29246444
[Au] Autor:Riquelme SA; Hopkins BD; Wolfe AL; DiMango E; Kitur K; Parsons R; Prince A
[Ad] Endereço:Department of Pediatrics, Columbia University, New York, NY 10032, USA.
[Ti] Título:Cystic Fibrosis Transmembrane Conductance Regulator Attaches Tumor Suppressor PTEN to the Membrane and Promotes Anti Pseudomonas aeruginosa Immunity.
[So] Source:Immunity;47(6):1169-1181.e7, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor suppressor PTEN controls cell proliferation by regulating phosphatidylinositol-3-kinase (PI3K) activity, but the participation of PTEN in host defense against bacterial infection is less well understood. Anti-inflammatory PI3K-Akt signaling is suppressed in patients with cystic fibrosis (CF), a disease characterized by hyper-inflammatory responses to airway infection. We found that Ptenl mice, which lack the NH -amino terminal splice variant of PTEN, were unable to eradicate Pseudomonas aeruginosa from the airways and could not generate sufficient anti-inflammatory PI3K activity, similar to what is observed in CF. PTEN and the CF transmembrane conductance regulator (CFTR) interacted directly and this interaction was necessary to position PTEN at the membrane. CF patients under corrector-potentiator therapy, which enhances CFTR transport to the membrane, have increased PTEN amounts. These findings suggest that improved CFTR trafficking could enhance P. aeruginosa clearance from the CF airway by activating PTEN-mediated anti-bacterial responses and might represent a therapeutic strategy.
[Mh] Termos MeSH primário: Membrana Celular/imunologia
Regulador de Condutância Transmembrana em Fibrose Cística/imunologia
Fibrose Cística/imunologia
PTEN Fosfo-Hidrolase/imunologia
Infecções por Pseudomonas/imunologia
[Mh] Termos MeSH secundário: Aminofenóis/farmacologia
Aminopiridinas/farmacologia
Animais
Benzodioxóis/farmacologia
Membrana Celular/efeitos dos fármacos
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Fibrose Cística/microbiologia
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Regulação da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Modelos Moleculares
Monócitos/efeitos dos fármacos
Monócitos/imunologia
Monócitos/microbiologia
PTEN Fosfo-Hidrolase/deficiência
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinases/genética
Fosfatidilinositol 3-Quinases/imunologia
Ligação Proteica
Conformação Proteica
Transporte Proteico
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/imunologia
Infecções por Pseudomonas/genética
Infecções por Pseudomonas/microbiologia
Pseudomonas aeruginosa/imunologia
Quinolonas/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (CFTR protein, human); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human); EC 3.1.3.67 (Pten protein, mouse); EGP8L81APK (lumacaftor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


  9 / 3709 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29232554
[Au] Autor:Gong X; Litchfield LM; Webster Y; Chio LC; Wong SS; Stewart TR; Dowless M; Dempsey J; Zeng Y; Torres R; Boehnke K; Mur C; Marugán C; Baquero C; Yu C; Bray SM; Wulur IH; Bi C; Chu S; Qian HR; Iversen PW; Merzoug FF; Ye XS; Reinhard C; De Dios A; Du J; Caldwell CW; Lallena MJ; Beckmann RP; Buchanan SG
[Ad] Endereço:Eli Lilly and Company, Indianapolis, IN 46285, USA.
[Ti] Título:Genomic Aberrations that Activate D-type Cyclins Are Associated with Enhanced Sensitivity to the CDK4 and CDK6 Inhibitor Abemaciclib.
[So] Source:Cancer Cell;32(6):761-776.e6, 2017 Dec 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most cancers preserve functional retinoblastoma (Rb) and may, therefore, respond to inhibition of D-cyclin-dependent Rb kinases, CDK4 and CDK6. To date, CDK4/6 inhibitors have shown promising clinical activity in breast cancer and lymphomas, but it is not clear which additional Rb-positive cancers might benefit from these agents. No systematic survey to compare relative sensitivities across tumor types and define molecular determinants of response has been described. We report a subset of cancers highly sensitive to CDK4/6 inhibition and characterized by various genomic aberrations known to elevate D-cyclin levels and describe a recurrent CCND1 3'UTR mutation associated with increased expression in endometrial cancer. The results suggest multiple additional classes of cancer that may benefit from CDK4/6-inhibiting drugs such as abemaciclib.
[Mh] Termos MeSH primário: Aminopiridinas/farmacologia
Benzimidazóis/farmacologia
Ciclina D/metabolismo
Neoplasias/genética
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Proliferação Celular/efeitos dos fármacos
Ensaios Clínicos Fase I como Assunto
Ciclina D/genética
Quinase 4 Dependente de Ciclina/antagonistas & inibidores
Quinase 6 Dependente de Ciclina/antagonistas & inibidores
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-(4-ethylpiperazin-1-ylmethyl)pyridin-2-yl)-(5-fluoro-4-(7-fluoro-3-isopropyl-2-methyl-3H-benzimidazol-5-yl)pyrimidin-2-yl)amine); 0 (Aminopyridines); 0 (Antineoplastic Agents); 0 (Benzimidazoles); 0 (Cyclin D); EC 2.7.11.22 (Cyclin-Dependent Kinase 4); EC 2.7.11.22 (Cyclin-Dependent Kinase 6)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  10 / 3709 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29209709
[Au] Autor:Cutting GR
[Ad] Endereço:McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Título:Treating Specific Variants Causing Cystic Fibrosis.
[So] Source:JAMA;318(21):2130-2131, 2017 12 05.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Aminofenóis/uso terapêutico
Aminopiridinas/uso terapêutico
Benzodioxóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Fibrose Cística/tratamento farmacológico
Quinolonas/uso terapêutico
[Mh] Termos MeSH secundário: Fibrose Cística/genética
Combinação de Medicamentos
Variação Genética
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminophenols); 0 (Aminopyridines); 0 (Benzodioxoles); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Drug Combinations); 0 (Quinolones); 0 (lumacaftor, ivacaftor drug combination); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.16823



página 1 de 371 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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