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  1 / 19729 MEDLINE  
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[PMID]:29363351
[Au] Autor:Faghfuri E; Nikfar S; Niaz K; Faramarzi MA; Abdollahi M
[Ad] Endereço:a Pharmaceutical Biotechnology, Faculty of Pharmacy , Tehran University of Medical Sciences , Tehran , Iran.
[Ti] Título:Mitogen-activated protein kinase (MEK) inhibitors to treat melanoma alone or in combination with other kinase inhibitors.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):317-330, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Malignant melanoma (MM) is an aggressive disease with a rapidly rising incidence due to neoplasm of melanocytes. Molecular targeted therapies have demonstrated lower toxicity and improved overall survival versus conventional therapies of MM. The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM. Though, progression of resistance to these agents has prompted attempts to target downstream proteins in this pathway. Trametinib, a MEK1/2 inhibitor, was approved in 2013 for the treatment of BRAF V600E/K mutation-positive unresectable or metastatic cutaneous melanoma patients. Areas covered: The aim of the current review is to present an update on the role of MEK in progressive melanomas and summarize latest results of clinical studies with innovative MEK inhibitors and/or combined approaches with other kinase inhibitors such as BRAF inhibitors in the treatment of MM. Expert opinion: Two combined treatments (i.e. trametinib plus dabrafenib and vemurafenib plus cobimetinib) target two different kinases in the BRAF/MEK/ERK pathway. The simultaneous prohibition of both MEK and BRAF is associated with more durable response rate than BRAF monotherapy and can overcome acquired resistance.
[Mh] Termos MeSH primário: Melanoma/tratamento farmacológico
Inibidores de Proteínas Quinases/administração & dosagem
Neoplasias Cutâneas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Melanoma/genética
Melanoma/patologia
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Terapia de Alvo Molecular
Mutação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432593


  2 / 19729 MEDLINE  
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[PMID]:29322203
[Au] Autor:Dada R
[Ad] Endereço:Department of Oncology MBC J-64, King Faisal Specialist Hospital and Research Center, P.O. Box 40047, Jeddah, 21499, Kingdom of Saudi Arabia. rdada@kfshrc.edu.sa.
[Ti] Título:Program death inhibitors in classical Hodgkin's lymphoma: a comprehensive review.
[So] Source:Ann Hematol;97(4):555-561, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Cancer cells are able to induce immune system tolerance through different mechanisms. Recent achievements in the understanding of tumor microenvironment, invasion, and metastasizing have contributed to accelerated drug developments and approvals. Hodgkin lymphoma (HL) cells are the minority in a lymphocyte-rich microenvironment of HL tissue. The program death-1 (PD-1)/PD-ligand-1 checkpoint is one of the known effective pathways in classical HL to escape the immune system cells. The approval of PD-1 inhibitors in different cancer types with exciting response rates is truly revolutionizing our treatment armamentarium against cancer in general and classical HL in specific. Although the disease is one of the most curable tumors, we still need better outcome with more gentle treatment, especially for relapsed and refractory (r/r) patients. In this article, we review the current literature on immune checkpoint inhibitors and currently ongoing studies with nivolumab and pembrolizumab in r/r classical HL.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Antígeno B7-H1/antagonistas & inibidores
Doença de Hodgkin/tratamento farmacológico
Proteínas de Neoplasias/antagonistas & inibidores
Receptor de Morte Celular Programada 1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Anticorpos Monoclonais Humanizados/efeitos adversos
Anticorpos Monoclonais Humanizados/uso terapêutico
Antineoplásicos/efeitos adversos
Antineoplásicos Imunológicos/efeitos adversos
Antineoplásicos Imunológicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Antígeno B7-H1/metabolismo
Aprovação de Drogas
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Doença de Hodgkin/metabolismo
Seres Humanos
Terapia de Alvo Molecular/efeitos adversos
Proteínas de Neoplasias/metabolismo
Receptor de Morte Celular Programada 1/metabolismo
Qualidade de Vida
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (Antineoplastic Agents, Immunological); 0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (Neoplasm Proteins); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 31YO63LBSN (nivolumab); DPT0O3T46P (pembrolizumab)
[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:180112
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3226-0


  3 / 19729 MEDLINE  
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[PMID]:29268133
[Au] Autor:Zhu G; Xu Y; Cen X; Nandakumar KS; Liu S; Cheng K
[Ad] Endereço:Guangdong Provincial Key Laboratory of New Drug Screening and Guangzhou Key Laboratory of Drug Research for Emerging Virus Prevention and Treatment, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
[Ti] Título:Targeting pattern-recognition receptors to discover new small molecule immune modulators.
[So] Source:Eur J Med Chem;144:82-92, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Pattern recognition receptors (PRRs) are key immune receptors of the innate immune system, which recognize the conserved pathogen-associated molecular patterns (PAMPs) of the invading pathogens. Compared to the adaptive immune receptors, PRRs have three distinguishing features, viz., universal expression, fast response and recognizing many kinds of microbes. Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs) and NOD-like receptors (NLRs) recognize viral nucleic acid/bacterial fragments and trigger anti-microbial innate immune responses. Upon recognition of their ligand species, PRRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in the activation of nuclear factor-κB (NF-κB), mitogen-activated protein (MAP) kinases and interferon regulatory factors (IRFs) that control the transcription of genes encoding pro-inflammatory factors including type I interferon and other inflammatory cytokines, which are critical for eliminating the potential threat to the host. Here, we summarize the effects of small molecule regulators acting on signaling pathways initiated by TLR, RLR and NLR as well as their influence on innate and adaptive immune responses leading to therapy.
[Mh] Termos MeSH primário: Imunidade Adaptativa/efeitos dos fármacos
Imunidade Inata/efeitos dos fármacos
Fatores Imunológicos/química
Fatores Imunológicos/farmacologia
Receptores de Reconhecimento de Padrão/imunologia
[Mh] Termos MeSH secundário: Animais
Descoberta de Drogas
Seres Humanos
Inflamação/tratamento farmacológico
Inflamação/imunologia
Terapia de Alvo Molecular
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Receptors, Pattern Recognition); 0 (Small Molecule Libraries)
[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:171222
[St] Status:MEDLINE


  4 / 19729 MEDLINE  
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[PMID]:29288362
[Au] Autor:Goonesekere NCW; Andersen W; Smith A; Wang X
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Northern Iowa, 1227 W. 27th Street, Cedar Falls, IA, 50613-0423, USA. nalin.goonesekere@uni.edu.
[Ti] Título:Identification of genes highly downregulated in pancreatic cancer through a meta-analysis of microarray datasets: implications for discovery of novel tumor-suppressor genes and therapeutic targets.
[So] Source:J Cancer Res Clin Oncol;144(2):309-320, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The lack of specific symptoms at early tumor stages, together with a high biological aggressiveness of the tumor contribute to the high mortality rate for pancreatic cancer (PC), which has a 5-year survival rate of about 7%. Recent failures of targeted therapies inhibiting kinase activity in clinical trials have highlighted the need for new approaches towards combating this deadly disease. METHODS: In this study, we have identified genes that are significantly downregulated in PC, through a meta-analysis of large number of microarray datasets. We have used qRT-PCR to confirm the downregulation of selected genes in a panel of PC cell lines. RESULTS: This study has yielded several novel candidate tumor-suppressor genes (TSGs) including GNMT, CEL, PLA2G1B and SERPINI2. We highlight the role of GNMT, a methyl transferase associated with the methylation potential of the cell, and CEL, a lipase, as potential therapeutic targets. We have uncovered genetic links to risk factors associated with PC such as smoking and obesity. Genes important for patient survival and prognosis are also discussed, and we confirm the dysregulation of metabolic pathways previously observed in PC. CONCLUSIONS: While many of the genes downregulated in our dataset are associated with protein products normally produced by the pancreas for excretion, we have uncovered some genes whose downregulation appear to play a more causal role in PC. These genes will assist in providing a better understanding of the disease etiology of PC, and in the search for new therapeutic targets and biomarkers.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
Neoplasias Pancreáticas/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Conjuntos de Dados como Assunto
Regulação para Baixo
Seres Humanos
Terapia de Alvo Molecular
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2558-4


  5 / 19729 MEDLINE  
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[PMID]:29191878
[Au] Autor:Klaeger S; Heinzlmeir S; Wilhelm M; Polzer H; Vick B; Koenig PA; Reinecke M; Ruprecht B; Petzoldt S; Meng C; Zecha J; Reiter K; Qiao H; Helm D; Koch H; Schoof M; Canevari G; Casale E; Depaolini SR; Feuchtinger A; Wu Z; Schmidt T; Rueckert L; Becker W; Huenges J; Garz AK; Gohlke BO; Zolg DP; Kayser G; Vooder T; Preissner R; Hahne H; Tõnisson N; Kramer K; Götze K; Bassermann F; Schlegl J; Ehrlich HC; Aiche S; Walch A; Greif PA; Schneider S; Felder ER; Ruland J; Médard G; Jeremias I; Spiekermann K; Kuster B
[Ad] Endereço:Chair of Proteomics and Bioanalytics, Technical University of Munich (TUM), Freising, Germany.
[Ti] Título:The target landscape of clinical kinase drugs.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kinase inhibitors are important cancer therapeutics. Polypharmacology is commonly observed, requiring thorough target deconvolution to understand drug mechanism of action. Using chemical proteomics, we analyzed the target spectrum of 243 clinically evaluated kinase drugs. The data revealed previously unknown targets for established drugs, offered a perspective on the "druggable" kinome, highlighted (non)kinase off-targets, and suggested potential therapeutic applications. Integration of phosphoproteomic data refined drug-affected pathways, identified response markers, and strengthened rationale for combination treatments. We exemplify translational value by discovering SIK2 (salt-inducible kinase 2) inhibitors that modulate cytokine production in primary cells, by identifying drugs against the lung cancer survival marker MELK (maternal embryonic leucine zipper kinase), and by repurposing cabozantinib to treat FLT3-ITD-positive acute myeloid leukemia. This resource, available via the ProteomicsDB database, should facilitate basic, clinical, and drug discovery research and aid clinical decision-making.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Descoberta de Drogas/métodos
Terapia de Alvo Molecular
Inibidores de Proteínas Quinases/farmacologia
Proteômica/métodos
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Linhagem Celular Tumoral
Citocinas/metabolismo
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/enzimologia
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/enzimologia
Camundongos
Inibidores de Proteínas Quinases/química
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
Tirosina Quinase 3 Semelhante a fms/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (Protein Kinase Inhibitors); EC 2.7.1.- (MELK protein, human); EC 2.7.1.- (salt-inducible kinase-2, human); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


  6 / 19729 MEDLINE  
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[PMID]:28463413
[Au] Autor:da Silveira Nogueira Lima JP; Georgieva M; Haaland B; de Lima Lopes G
[Ad] Endereço:Drug Development Unit, Institute of Cancer Research, Sutton, United Kingdom.
[Ti] Título:A systematic review and network meta-analysis of immunotherapy and targeted therapy for advanced melanoma.
[So] Source:Cancer Med;6(6):1143-1153, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immune and BRAF-targeted therapies have changed the therapeutic scenario of advanced melanoma, turning the clinical decision-making a challenging task. This Bayesian network meta-analysis assesses the role of immunotherapies and targeted therapies for advanced melanoma. We retrieved randomized controlled trials testing immune, BRAF- or MEK-targeted therapies for advanced melanoma from electronic databases. A Bayesian network model compared therapies using hazard ratio (HR) for overall survival (OS), progression-free survival (PFS), and odds ratio (OR) for response rate (RR), along with 95% credible intervals (95% CrI), and probabilities of drugs outperforming others. We assessed the impact of PD-L1 expression on immunotherapy efficacy. Sixteen studies evaluating eight therapies in 6849 patients were analyzed. For OS, BRAF-MEK combination and PD-1 single agent ranked similarly and outperformed all other treatments. For PFS, BRAF-MEK combination surpassed all other options, including CTLA-4-PD-1 dual blockade hazard ratio (HR: 0.56; 95% CrI: 0.33-0.97; probability better 96.2%), whereas BRAF single agent ranked close to CTLA-4-PD-1 blockade. For RR, BRAF-MEK combination was superior to all treatments including CTLA-4-PD-1 (OR: 2.78; 1.18-6.30; probability better 97.1%). No OS data were available for CTLA-4-PD-1 blockade at the time of systematic review, although PFS and RR results suggested that this combination could also bring meaningful benefit. PD-L1 expression, as presently defined, failed to inform patient selection to PD-1-based immunotherapy. BRAF-MEK combination seemed an optimal therapy for BRAF-mutated patients, whereas PD-1 inhibitors seemed optimal for BRAF wild-type patients. Longer follow-up is needed to ascertain the role of CTLA-4-PD-1 blockade. Immunotherapy biomarkers remain as an unmet need.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/uso terapêutico
Imunoterapia
Melanoma/terapia
Terapia de Alvo Molecular
[Mh] Termos MeSH secundário: Intervalo Livre de Doença
Seres Humanos
Melanoma/tratamento farmacológico
Ensaios Clínicos Controlados Aleatórios como Assunto
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.1001


  7 / 19729 MEDLINE  
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[PMID]:29325268
[Au] Autor:Li MJ; Li HR; Cheng X; Bi R; Tu XY; Liu F; Chen LH
[Ad] Endereço:Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
[Ti] Título:[Clinical significance of targeting drug-based molecular biomarkers expression in ovarian clear cell carcinoma].
[So] Source:Zhonghua Fu Chan Ke Za Zhi;52(12):835-843, 2017 Dec 25.
[Is] ISSN:0529-567X
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To assess the expression level of targeting drug-based molecular biomarkers in ovarian clear cell carcinoma (OCCC) tissues and its clinical significance. A total of 63 OCCC patients included 40 primary OCCC and 23 recurrent OCCC for secondary cytoreductive surgery (SCS), who had received primary surgeries at Fudan University Shanghai Cancer Center between January, 2008 and December, 2015 were enrolled, and immunohistochemistry SP method was used to test human epidermal growth factor receptor (EGFR), human epidermal growth factor receptor-2 (HER2), aurora kinase A (AURKA), breast cancer susceptibility gene 1 (BRCA1), BRCA2 and programmed death-ligand 1 (PD-L1)protein expression in paraffin-embedded tissues. The positive rates of EGFR, HER2, AURKA,BRCA1, BRCA2 and PD-L1 in primary and recurrent tumor tissues were respectively 20% (8/40) vs 30% (7/23) , 22% (9/40) vs 35% (8/23) , 38% (15/40) vs 35% (8/23) , 42% (17/40) vs 39% (9/23) , 20% (8/40) vs 22% (5/23) , 25% (10/40) vs 17% (4/23) , and there were no significant differences between primary and recurrent OCCC (all 0.05). χ(2)-test or Fisher exact analysis revealed that HER2 expression in recurrent tumor tissues had a relationship with chemoresistance ( 0.05), while the expression of other biomarkers showed no significant relationship with chemoresistance (all 0.05). Further, Kaplan-Meier survival analysis showed that patients with HER2 and AURKA-positive expression had a significantly shorter progression-free survival time in primary OCCC (4 months vs 10 months, log-rank test, 0.05 for HER2; and 4 months vs 10 months, 0.05 for AURKA); and a shorter overall survival time after SCS in recurrent OCCC (10 months vs 44 months, 0.05 for HER2; and 13 months vs 43 months, 0.05 for AURKA). However, multivariate Cox proportional hazards regression analysis indicated that none of these 6 biomarkers was independent risk factor of progression-free survival time of primary OCCC or overall survival time after SCS for recurrent OCCC ( 0.05). HER2 and AURKA could serve as prognostic factors in ovarian clear cell carcinoma.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/tratamento farmacológico
Adenocarcinoma de Células Claras/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/metabolismo
Medicina de Precisão
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/diagnóstico
Adenocarcinoma de Células Claras/mortalidade
Proteína BRCA2
China
Intervalo Livre de Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Terapia de Alvo Molecular
Recidiva Local de Neoplasia
Neoplasias Epiteliais e Glandulares/diagnóstico
Neoplasias Epiteliais e Glandulares/mortalidade
Neoplasias Ovarianas/diagnóstico
Neoplasias Ovarianas/mortalidade
Receptor do Fator de Crescimento Epidérmico
Receptor ErbB-2
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (Biomarkers, Tumor); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-567x.2017.12.008


  8 / 19729 MEDLINE  
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[PMID]:28453233
[Au] Autor:Huang YP; Chang NW
[Ad] Endereço:Department of Physiology, College of Medicine, China Medical University, Taichung, Taiwan.
[Ti] Título:Proteomic analysis of oral cancer reveals new potential therapeutic targets involved in the Warburg effect.
[So] Source:Clin Exp Pharmacol Physiol;44(8):880-887, 2017 Aug.
[Is] ISSN:1440-1681
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Activation of peroxisome proliferator-activated receptor alpha (PPARα) has been reported to disrupt tumour metabolism and to promote anticancer activity through interfering with the Warburg effect. This study is to investigate whether Warburg effect-related proteins also could be identified in oral tumour lesions and to explore the functional significance of PPARα in metabolic shift. Five pairs of tongue tumour tissues and adjacent reference tissues obtained from 4-NQO/arecoline induced mouse model were analyzed by 2-d-gel-electrophoresis and LC-MS. Further, the hexokinase II level, pyruvate dehydrogenase (PDH) activity, and metabolites of glycolysis and TCA cycle were all examined in order to validate the effect of PPARα on metabolic shift. Changes in protein expression levels revealed that seven proteins, which were involved in glycolysis, the tricarboxylic acid cycle, and the respiratory chain, were down-regulated in tumour tissues. We found that activation of PPARα through fenofibrate could inhibit oral cancer cell growth and switch the way of energy production from the Warburg effect to oxidative phosphorylation. Fenofibrate induced a reduction of hexokinase II protein levels, increases in PDH activity and metabolites of the TCA cycle, and an impairment of ATP production. These findings suggested that activation of the PPARα to reprogram the metabolic pathway might impair the Warburg effect and trigger cancer cell death. The study provides a novel view of changes in protein expression profiles involved in the Warburg effect during oral tumourigenesis. Activation of the PPARα to impair the Warburg effect might offer a new strategy for oral cancer treatment.
[Mh] Termos MeSH primário: Terapia de Alvo Molecular
Neoplasias Bucais/tratamento farmacológico
Neoplasias Bucais/metabolismo
Proteômica
[Mh] Termos MeSH secundário: Animais
Ciclo do Ácido Cítrico/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Bucais/patologia
Fosforilação Oxidativa/efeitos dos fármacos
PPAR alfa/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/1440-1681.12774


  9 / 19729 MEDLINE  
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[PMID]:27773806
[Au] Autor:Wooden B; Goossens N; Hoshida Y; Friedman SL
[Ad] Endereço:Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
[Ti] Título:Using Big Data to Discover Diagnostics and Therapeutics for Gastrointestinal and Liver Diseases.
[So] Source:Gastroenterology;152(1):53-67.e3, 2017 Jan.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Technologies such as genome sequencing, gene expression profiling, proteomic and metabolomic analyses, electronic medical records, and patient-reported health information have produced large amounts of data from various populations, cell types, and disorders (big data). However, these data must be integrated and analyzed if they are to produce models or concepts about physiological function or mechanisms of pathogenesis. Many of these data are available to the public, allowing researchers anywhere to search for markers of specific biological processes or therapeutic targets for specific diseases or patient types. We review recent advances in the fields of computational and systems biology and highlight opportunities for researchers to use big data sets in the fields of gastroenterology and hepatology to complement traditional means of diagnostic and therapeutic discovery.
[Mh] Termos MeSH primário: Biologia Computacional
Descoberta de Drogas/métodos
Gastroenteropatias/diagnóstico
Gastroenteropatias/tratamento farmacológico
Hepatopatias/diagnóstico
Hepatopatias/tratamento farmacológico
[Mh] Termos MeSH secundário: Biomarcadores
Mineração de Dados
Seres Humanos
Terapia de Alvo Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29381393
[Au] Autor:Ding M; Pan J; Guo Z; Liu Q; Yang C; Mao L
[Ad] Endereço:a Jiangsu Key Laboratory of Biological Cancer Therapy, Xuzhou University , Xuzhou , China.
[Ti] Título:SATB1 is a Novel Molecular Target for Cancer Therapy.
[So] Source:Cancer Invest;36(1):28-36, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The special AT-rich sequence binding-protein1 (SATB1) attracts excessive attention due to its high expression in a variety of malignancies. SATB1 reprograms chromatin and transcription profiles to promote tumor cell growth and invasion and inhibit apoptosis, leading to tumor progression and metastasis. Consistently, silencing SATB1 with small interfering RNA inhibits the growth and invasion of some kinds of tumors. In this review, we highlight recent progress in our understanding of the role of SATB1 as global regulator of gene expression during cancer development, and evaluate the potential of SATB1 as a molecular therapeutic target for cancers with aberrant SATB1 expression.
[Mh] Termos MeSH primário: Proteínas de Ligação à Região de Interação com a Matriz/genética
Neoplasias/genética
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/genética
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Terapia de Alvo Molecular/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Matrix Attachment Region Binding Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2018.1423688



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