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[PMID]:29388834
[Au] Autor:Oldham WM
[Ad] Endereço:1 Department of Medicine Brigham and Women's Hospital and Harvard Medical School Boston, Massachusetts.
[Ti] Título:The Long Noncoding RNA LnRPT Puts the Brakes on Pulmonary Artery Smooth Muscle Cell Proliferation.
[So] Source:Am J Respir Cell Mol Biol;58(2):138-139, 2018 02.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Hipertensão Pulmonar/patologia
Miócitos de Músculo Liso/citologia
Artéria Pulmonar/citologia
RNA Longo não Codificante/genética
Resistência Vascular/fisiologia
[Mh] Termos MeSH secundário: Proliferação Celular/genética
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/prevenção & controle
Seres Humanos
Pulmão/irrigação sanguínea
Músculo Liso Vascular/citologia
Receptores do Fator de Crescimento Derivado de Plaquetas/fisiologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (RNA, Long Noncoding); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0342ED


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[PMID]:29277808
[Au] Autor:Poprach A; Fiala O; Chloupkova R; Melichar B; Lakomy R; Petrakova K; Zemanova M; Kopeckova K; Slaby O; Studentova H; Kopecký J; Kiss I; Finek J; Dusek L; Buchler T
[Ad] Endereço:Department of Comprehensive Cancer Care, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
[Ti] Título:Pazopanib for Metastatic Renal Cell Carcinoma: A Registry-based Analysis of 426 Patients.
[So] Source:Anticancer Res;38(1):449-456, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pazopanib is approved for the first-line treatment of patients with metastatic renal cell carcinoma (mRCC). The present study was a retrospective registry-based analysis of 426 patients with mRCC treated with pazopanib as first-line targeted therapy. PATIENTS AND METHODS: The data were obtained from the Renal Cell Carcinoma Information system registry. Patient baseline parameters, treatment course and outcomes, and toxicity were analysed. RESULTS: Median progression-free and overall survival were 12.9 (95% confidence interval(CI)=11.0-14.8) months and 33.2 (95% CI=29.9-36.4) months, respectively. Overall response rate and disease control rate were 25.1% and 57.4%, respectively. Adverse events led to discontinuation of treatment in 37 (12.1%) patients. CONCLUSION: The results confirm that pazopanib is an effective and safe first-line targeted treatment in patients with mRCC. Both the International mRCC Database Consortium and the Memorial Sloan Kettering models were valid predictors of prognosis and nephrectomy was associated with improved survival.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/uso terapêutico
Carcinoma de Células Renais/tratamento farmacológico
Neoplasias Renais/tratamento farmacológico
Pirimidinas/uso terapêutico
Sulfonamidas/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Inibidores da Angiogênese/efeitos adversos
Carcinoma de Células Renais/patologia
Carcinoma de Células Renais/cirurgia
República Tcheca
Bases de Dados Factuais
Intervalo Livre de Doença
Feminino
Seres Humanos
Indóis/uso terapêutico
Neoplasias Renais/patologia
Neoplasias Renais/cirurgia
Masculino
Meia-Idade
Nefrectomia
Proteínas Proto-Oncogênicas c-kit/antagonistas & inibidores
Pirimidinas/efeitos adversos
Pirróis/uso terapêutico
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Receptores de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Sistema de Registros
Estudos Retrospectivos
Sulfonamidas/efeitos adversos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Indoles); 0 (Pyrimidines); 0 (Pyrroles); 0 (Sulfonamides); 7RN5DR86CK (pazopanib); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor); V99T50803M (sunitinib)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29211993
[Au] Autor:Buckles TC; Ziemba BP; Masson GR; Williams RL; Falke JJ
[Ad] Endereço:Molecular Biophysics Program and Department of Chemistry and Biochemistry, University of Colorado, Boulder, Colorado.
[Ti] Título:Single-Molecule Study Reveals How Receptor and Ras Synergistically Activate PI3Kα and PIP Signaling.
[So] Source:Biophys J;113(11):2396-2405, 2017 Dec 05.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cellular pathways controlling chemotaxis, growth, survival, and oncogenesis are activated by receptor tyrosine kinases and small G-proteins of the Ras superfamily that stimulate specific isoforms of phosphatidylinositol-3-kinase (PI3K). These PI3K lipid kinases phosphorylate the constitutive lipid phosphatidylinositol-4,5-bisphosphate (PIP ) to produce the signaling lipid phosphatidylinositol-3,4,5-trisphosphate (PIP ). Progress has been made in understanding direct, moderate PI3K activation by receptors. In contrast, the mechanism by which receptors and Ras synergistically activate PI3K to much higher levels remains unclear, and two competing models have been proposed: membrane recruitment versus activation of the membrane-bound enzyme. To resolve this central mechanistic question, this study employs single-molecule imaging to investigate PI3K activation in a six-component pathway reconstituted on a supported lipid bilayer. The findings reveal that simultaneous activation by a receptor activation loop (from platelet-derived growth factor receptor, a receptor tyrosine kinase) and H-Ras generates strong, synergistic activation of PI3Kα, yielding a large increase in net kinase activity via the membrane recruitment mechanism. Synergy requires receptor phospho-Tyr and two anionic lipids (phosphatidylserine and PIP ) to make PI3Kα competent for bilayer docking, as well as for subsequent binding and phosphorylation of substrate PIP to generate product PIP . Synergy also requires recruitment to membrane-bound H-Ras, which greatly speeds the formation of a stable, membrane-bound PI3Kα complex, modestly slows its off rate, and dramatically increases its equilibrium surface density. Surprisingly, H-Ras binding significantly inhibits the specific kinase activity of the membrane-bound PI3Kα molecule, but this minor enzyme inhibition is overwhelmed by the marked enhancement of membrane recruitment. The findings have direct impacts for the fields of chemotaxis, innate immunity, inflammation, carcinogenesis, and drug design.
[Mh] Termos MeSH primário: Fosfatidilinositol 3-Quinases/metabolismo
Fosfatos de Fosfatidilinositol/metabolismo
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
Transdução de Sinais
Proteínas ras/metabolismo
[Mh] Termos MeSH secundário: Ativação Enzimática
Bicamadas Lipídicas/metabolismo
Microscopia de Fluorescência
Modelos Moleculares
Fosfatidilinositol 3-Quinases/química
Fosfopeptídeos/metabolismo
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipid Bilayers); 0 (Phosphatidylinositol Phosphates); 0 (Phosphopeptides); 0 (phosphatidylinositol 3,4,5-triphosphate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


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[PMID]:28649871
[Au] Autor:Rossi A; Latiano TP; Parente P; Chiarazzo C; Limosani F; Di Maggio G; Maiello E
[Ad] Endereço:a Oncology Unit , IRCCS Casa Sollievo della Sofferenza Hospital , San Giovanni Rotondo , Italy.
[Ti] Título:The potential role of nintedanib in treating colorectal cancer.
[So] Source:Expert Opin Pharmacother;18(11):1153-1162, 2017 Aug.
[Is] ISSN:1744-7666
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Angiogenesis leads to the growth, progression, and metastases of a variety of solid tumors, including metastatic colorectal cancer (mCRC), involving particularly the family of vascular endothelial growth factors (VEGF) and their receptors (VEGFR). Several anti-angiogenic inhibitors are already registered for mCRC therapy: bevacizumab, aflibercept, ramucirumab, regorafenib. Nintedanib is a new triple angiokinase oral inhibitor that potently blocks the proangiogenic pathways mediated by VEGFR, platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR). Areas covered: The current state-of-the-art of anti-angiogenic inhibitors employed in the treatment mCRC patients, and in particular the role of nintedanib in this setting, is reviewed and discussed here. A structured search of bibliographic databases for peer-reviewed research literature and of main meetings using a focused review question was undertaken. Expert opinion: In first-line therapy, a phase II randomized trial showed that nintedanib plus chemotherapy was not inferior to the bevacizumab-based regimen. In heavily pretreated mCRC patients nintedanib improved some outcomes. During the natural history of mCRC resistances to anti-angiogenic therapies can set in and in this context, nintedanib, due to its triple inhibition, might play a role in compensatory angiogenesis overcoming the resistance developed due to VEGF directed therapy.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/uso terapêutico
Neoplasias Colorretais/tratamento farmacológico
Indóis/uso terapêutico
Neovascularização Patológica/tratamento farmacológico
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/administração & dosagem
Inibidores da Angiogênese/efeitos adversos
Neoplasias Colorretais/irrigação sanguínea
Neoplasias Colorretais/patologia
Seres Humanos
Indóis/administração & dosagem
Indóis/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto
Receptores de Fatores de Crescimento de Fibroblastos/antagonistas & inibidores
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Resultado do Tratamento
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Indoles); 0 (Receptors, Fibroblast Growth Factor); EC 2.7.10.1 (FLT1 protein, human); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1); G6HRD2P839 (nintedanib)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1080/14656566.2017.1346086


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[PMID]:28570599
[Au] Autor:Wang LX; Yang X; Yue Y; Fan T; Hou J; Chen GX; Liang MY; Wu ZK
[Ad] Endereço:Second Department of Cardiac Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:Imatinib attenuates cardiac fibrosis by inhibiting platelet-derived growth factor receptors activation in isoproterenol induced model.
[So] Source:PLoS One;12(6):e0178619, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiac fibrosis is a significant global health problem with limited treatment choices. Although previous studies have shown that imatinib (IMA) inhibited cardiac fibrosis, the anti-fibrotic mechanisms have not been clearly uncovered. The aim of this study is to evaluate whether IMA attenuates cardiac fibrosis by inhibiting platelet-derived growth factor receptors (PDGFR) on isoproterenol (ISO)-induced mice. Adult male C57BL/6 mice were treated with vehicle or ISO ± IMA for one week. After echocardiography examination, the hearts of mice were used for histopathologic, RT-qPCR, and western blot analyses. We found that the ventricular wall thickness, cardiac hypertrophy, and apoptosis were enhanced following ISO treatment. IMA decreased the left ventricular wall thickness, prevented hypertrophy, and inhibited apoptosis induced by ISO. In addition, IMA attenuated the accumulation of collagens and α-smooth muscle actin (α-SMA) (the markers of fibrosis) caused by ISO treatment. Moreover, the expression of fibrosis related genes, and the phosphorylation of PDGFRs in ISO-treated mice hearts were inhibited by IMA as well. However, IMA did not change the expression of the matrix metalloproteinase-9 (MMP-9) in ISO-treated hearts. Furthermore, IMA reduced the expressions of collagens as well as α-SMA caused by activation of PDGFRα in cardiac fibroblasts. Taken together, our data demonstrate that IMA attenuated the cardiac fibrosis by blocking the phosphorylation of PDGFRs in the ISO-induced mice model. This study indicates that IMA could be a potentially therapeutic option for cardiac fibrosis in clinical application.
[Mh] Termos MeSH primário: Cardiopatias/prevenção & controle
Mesilato de Imatinib/farmacologia
Isoproterenol/farmacologia
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Ecocardiografia
Fibrose/prevenção & controle
Expressão Gênica/efeitos dos fármacos
Cardiopatias/induzido quimicamente
Cardiopatias/diagnóstico por imagem
Cardiopatias/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fosforilação
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
Remodelação Ventricular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
8A1O1M485B (Imatinib Mesylate); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178619


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[PMID]:28506734
[Au] Autor:Kerr DA; Busarla SVP; Gimbel DC; Sohani AR; Nazarian RM
[Ad] Endereço:Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114. Electronic address: dkerr@med.miami.edu.
[Ti] Título:mTOR, VEGF, PDGFR, and c-kit signaling pathway activation in Kaposi sarcoma.
[So] Source:Hum Pathol;65:157-165, 2017 Jul.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kaposi sarcoma (KS) is a locally progressive, intermediate-grade vascular neoplasm with no known cure, high recurrence rates, and potential for wide dissemination. Low efficacy and high toxicity limit current therapeutic options for advanced disease. Activation of mammalian target of rapamycin (mTOR), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and c-kit signaling pathways has been implicated in KS pathogenesis and may suggest a role for targeted inhibitors. KS cases were retrospectively retrieved (N=274), most (90%) associated with human immunodeficiency virus. Tissue microarray slides were stained with human herpes virus-8, Friend leukemia integration 1 transcription factor, CD117 (c-kit), phospho-S6 (pS6), PDGF receptor-ß, VEGF, and phospho-mTOR. Both intensity and extent of staining were scored. Multiplying these scores for each core yielded total staining H-scores. Human herpes virus-8 was positive in 87% and Friend leukemia integration 1 transcription factor in 95.7% of cases. Most were also VEGF+ (97.6%), pS6+ (95.7%), CD117+ (92.5%), and PDGFRB+ (87.4%). Approximately half (55.6%) were phospho-mTOR+. There was no significant difference in staining among patients with low (<500 cells/mm ) or preserved CD4 T-cell counts. Immunohistochemistry confirms upregulation of the mTOR, PDGF, VEGF, and c-kit pathways in a large cohort of KS samples. Of proteins tested, pS6, downstream of mTOR, demonstrated the highest proportion of strong positivity (67.1%). These results support the possibility of using targeted inhibitors in KS. Overexpression was independent of CD4 count, suggesting that even patients with low counts may be targeted therapy candidates.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Proteínas Proto-Oncogênicas c-kit/análise
Receptores do Fator de Crescimento Derivado de Plaquetas/análise
Sarcoma de Kaposi/química
Transdução de Sinais
Serina-Treonina Quinases TOR/análise
Fator A de Crescimento do Endotélio Vascular/análise
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/uso terapêutico
Contagem de Linfócito CD4
Criança
Pré-Escolar
Feminino
Infecções por HIV/imunologia
Infecções por HIV/virologia
Herpesvirus Humano 8/isolamento & purificação
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Terapia de Alvo Molecular
Fosforilação
Valor Preditivo dos Testes
Proteínas Proto-Oncogênicas c-kit/antagonistas & inibidores
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Estudos Retrospectivos
Proteína S6 Ribossômica/análise
Sarcoma de Kaposi/tratamento farmacológico
Sarcoma de Kaposi/patologia
Sarcoma de Kaposi/virologia
Transdução de Sinais/efeitos dos fármacos
Serina-Treonina Quinases TOR/antagonistas & inibidores
Análise Serial de Tecidos
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Ribosomal Protein S6); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE


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[PMID]:28433542
[Au] Autor:Makino K; Makino T; Stawski L; Mantero JC; Lafyatis R; Simms R; Trojanowska M
[Ad] Endereço:Arthritis Center, Boston University School of Medicine, Boston, Massachusetts, USA.
[Ti] Título:Blockade of PDGF Receptors by Crenolanib Has Therapeutic Effect in Patient Fibroblasts and in Preclinical Models of Systemic Sclerosis.
[So] Source:J Invest Dermatol;137(8):1671-1681, 2017 Aug.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic sclerosis (SSc) is a multi-organ fibrotic disease with few treatment options. Activated fibroblasts are the key effector cells in SSc responsible for the excessive production of collagen and the development of fibrosis. Platelet-derived growth factor (PDGF), a potent mitogen for cells of mesenchymal origin, has been implicated in the activation of SSc fibroblasts. Our aim was to examine the therapeutic potential of crenolanib, an inhibitor of PDGF receptor signaling, in cultured fibroblasts and in angiotensin II-induced skin and heart fibrosis. Crenolanib effectively inhibited proliferation and migration of SSc and healthy control fibroblasts and attenuated basal and transforming growth factor-ß-induced expression of CCN2/CTGF and periostin. In contrast to healthy control fibroblasts, SSc fibroblasts proliferated in response to PDGFAA, whereas a combination of PDGFAA and CCN2 was required to elicit a similar response in healthy control fibroblasts. PDGF receptor α mRNA correlated with CCN2 and other fibrotic markers in the skin of SSc patients. In mice challenged with angiotensin II, PDGF receptor α-positive cells were increased in the skin and heart. These PDGF receptor α-positive cells co-localized with PDGF receptor ß, procollagen, and periostin. Treatment with crenolanib attenuated the skin and heart fibrosis. Our data indicate that inhibition of PDGF signaling presents an attractive therapeutic approach for SSc.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Piperidinas/farmacologia
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Escleroderma Sistêmico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Moléculas de Adesão Celular/biossíntese
Moléculas de Adesão Celular/genética
Células Cultivadas
Fator de Crescimento do Tecido Conjuntivo/biossíntese
Fator de Crescimento do Tecido Conjuntivo/genética
Modelos Animais de Doenças
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Fibroblastos/patologia
Regulação da Expressão Gênica
Seres Humanos
Immunoblotting
Camundongos
Camundongos Endogâmicos C57BL
RNA/genética
RNA Mensageiro
Reação em Cadeia da Polimerase em Tempo Real
Receptores do Fator de Crescimento Derivado de Plaquetas/biossíntese
Receptores do Fator de Crescimento Derivado de Plaquetas/genética
Escleroderma Sistêmico/metabolismo
Escleroderma Sistêmico/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Cell Adhesion Molecules); 0 (Ctgf protein, mouse); 0 (Piperidines); 0 (Postn protein, mouse); 0 (RNA, Messenger); 139568-91-5 (Connective Tissue Growth Factor); 63231-63-0 (RNA); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); LQF7I567TQ (crenolanib)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170424
[St] Status:MEDLINE


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[PMID]:28414915
[Au] Autor:Ackerman DS; Vasilev KV; Schmidt BF; Cohen LB; Jarvik JW
[Ad] Endereço:Department of Biological Sciences, ‡Department of Chemistry, and §Molecular Biosensor and Imaging Center, Carnegie Mellon University , 4400 Fifth Avenue, Pittsburgh, Pennsylvania 15213, United States.
[Ti] Título:Tethered Fluorogen Assay to Visualize Membrane Apposition in Living Cells.
[So] Source:Bioconjug Chem;28(5):1356-1362, 2017 May 17.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We describe proof-of-concept for a novel approach for visualizing regions of close apposition between the surfaces of living cells. A membrane-anchored protein with high affinity for a chemical ligand is expressed on the surface of one set of cells, and the cells are co-cultured with a second set of cells that express a membrane-anchored fluorogen-activating protein (FAP). The co-cultured cells are incubated with a bivalent reagent composed of fluorogen linked to the high-affinity ligand, with the concentration of the bivalent reagent chosen to be less than the binding constant for the FAP-fluorogen pair but greater than the binding constant for the ligand-high-affinity protein pair. In these conditions, strong FAP signal is observed only in regions of close proximity between membranes of the two classes of cell, where high local concentration of fluorogen favors binding to the FAP.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/metabolismo
Bioensaio/métodos
Técnicas Biossensoriais/métodos
Membrana Celular/metabolismo
Corantes Fluorescentes/química
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Microscopia de Fluorescência
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Fluorescent Dyes); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.7b00047


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[PMID]:28376230
[Au] Autor:Allen CE; Laetsch TW; Mody R; Irwin MS; Lim MS; Adamson PC; Seibel NL; Parsons DW; Cho YJ; Janeway K; Pediatric MATCH Target and Agent Prioritization Committee
[Ad] Endereço:Texas Children's Cancer Center, Texas Children's Hospital, Houston, TX, USA.
[Ti] Título:Target and Agent Prioritization for the Children's Oncology Group-National Cancer Institute Pediatric MATCH Trial.
[So] Source:J Natl Cancer Inst;109(5), 2017 05 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Over the past decades, outcomes for children with cancer have improved dramatically through serial clinical trials based in large measure on dose intensification of cytotoxic chemotherapy for children with high-risk malignancies. Progress made through such dose intensification, in general, is no longer yielding further improvements in outcome. With the revolution in sequencing technologies and rapid development of drugs that block specific proteins and pathways, there is now an opportunity to improve outcomes for pediatric cancer patients through mutation-based targeted therapeutic strategies. The Children's Oncology Group (COG), in partnership with the National Cancer Institute (NCI), is planning a trial entitled the COG-NCI Pediatric Molecular Analysis for Therapeutic Choice (Pediatric MATCH) protocol utilizing an umbrella design. This protocol will have centralized infrastructure and will consist of a biomarker profiling protocol and multiple single-arm phase II trials of targeted therapies. Pediatric patients with recurrent or refractory solid tumors, lymphomas, or histiocytoses with measurable disease will be eligible. The Pediatric MATCH Target and Agent Prioritization (TAP) committee includes membership representing COG disease committees, the Food and Drug Administration, and the NCI. The TAP Committee systematically reviewed target and agent pairs for inclusion in the Pediatric MATCH trial. Fifteen drug-target pairs were reviewed by the TAP Committee, with seven recommended for further development as initial arms of the Pediatric MATCH trial. The current evidence for availability, efficacy, and safety of targeted agents in children for each class of mutation considered for inclusion in the Pediatric MATCH trial is discussed in this review.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Terapia de Alvo Molecular
Neoplasias/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
[Mh] Termos MeSH secundário: Criança
Quinase 4 Dependente de Ciclina/antagonistas & inibidores
Quinase 6 Dependente de Ciclina/antagonistas & inibidores
Seres Humanos
MAP Quinase Quinase Quinases/antagonistas & inibidores
Proteínas Oncogênicas/antagonistas & inibidores
Fosfatidilinositol 3-Quinase/antagonistas & inibidores
Receptores Proteína Tirosina Quinases/antagonistas & inibidores
Receptores de Fatores de Crescimento de Fibroblastos/antagonistas & inibidores
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Projetos de Pesquisa
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Oncogene Proteins); 0 (Protein Kinase Inhibitors); 0 (Receptors, Fibroblast Growth Factor); 0 (oncogene protein trk); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); EC 2.7.10.1 (anaplastic lymphoma kinase); EC 2.7.11.22 (CDK6 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4); EC 2.7.11.22 (Cyclin-Dependent Kinase 6); EC 2.7.11.25 (MAP Kinase Kinase Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djw274


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[PMID]:28286261
[Au] Autor:Neri S; Miyashita T; Hashimoto H; Suda Y; Ishibashi M; Kii H; Watanabe H; Kuwata T; Tsuboi M; Goto K; Menju T; Sonobe M; Date H; Ochiai A; Ishii G
[Ad] Endereço:Division of Pathology, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan; Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, 54 Kawaharacho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan. Elec
[Ti] Título:Fibroblast-led cancer cell invasion is activated by epithelial-mesenchymal transition through platelet-derived growth factor BB secretion of lung adenocarcinoma.
[So] Source:Cancer Lett;395:20-30, 2017 Jun 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Cancer-associated fibroblast (CAF)-dependent local invasion is the process by which cancer cells invade the extracellular matrix using tracks that have been physically remodeled by CAFs. In the present study, we investigated the process by which the epithelial-mesenchymal transition (EMT) of cancer cells affect CAF-dependent local invasion. Using an in vitro collagen invasion assay, we showed cancer cells undergoing EMT to promote the matrix-remodeling ability of CAFs and thereby enhance CAF-dependent local cancer cell invasion. Platelet-derived growth factor (PDGF)-BB secretion was significantly elevated in cancer cells undergoing EMT, and this induced an increase in the invasion ability of both CAFs and cancer cells. Conversely, knockdown of PDGF-B expression in cancer cells undergoing EMT, or treatment with a PDGF-receptor inhibitor, decreased the invasion ability of both CAFs and cancer cells. By analyzing the gene expression profiles of 442 patients with lung adenocarcinomas, we established that high expression of PDGF-B and presentation of mesenchymal-like tumors were significantly associated with a high rate of disease recurrence and poor patient prognosis. Thus, cancer cells undergoing EMT may accelerate their own ability to invade local tissues via PDGF-BB secretion to promote CAF matrix remodeling. Therefore, targeting PDGF signaling between cancer cells undergoing EMT and CAFs is a promising therapeutic target to inhibit cancer progression and improve patient prognosis.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Fibroblastos Associados a Câncer/fisiologia
Transição Epitelial-Mesenquimal
Neoplasias Pulmonares/patologia
Proteínas Proto-Oncogênicas c-sis/fisiologia
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Células Cultivadas
Seres Humanos
Neoplasias Pulmonares/mortalidade
Invasividade Neoplásica
Receptores do Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-sis); 1B56C968OA (becaplermin); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE



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