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  1 / 2091 MEDLINE  
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[PMID]:27778377
[Au] Autor:Kyyriäinen J; Ekolle Ndode-Ekane X; Pitkänen A
[Ad] Endereço:Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, FI-70211, Finland.
[Ti] Título:Dynamics of PDGFRß expression in different cell types after brain injury.
[So] Source:Glia;65(2):322-341, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor receptor ß (PDGFRß) is upregulated after brain injury and its depletion results in the blood-brain barrier (BBB) damage. We investigated the time-window and localization of PDGFRß expression in mice with intrahippocampal kainic acid-induced status epilepticus (SE) and in rats with lateral fluid-percussion-induced traumatic brain injury (TBI). Tissue immunohistochemistry was evaluated at several time-points after SE and TBI. The distribution of PDGFRß was analyzed, and its cell type-specific expression was verified with double/triple-labeling of astrocytes (GFAP), NG2 cells, and endothelial cells (RECA-1). In normal mouse hippocampus, we found evenly distributed PDGFRß+ parenchymal cells. In double-labeling, all NG2+ and 40%-60% GFAP+ cells were PDGFRß+. After SE, PDGFRß+ cells clustered in the ipsilateral hilus (178% of that in controls at fourth day, 225% at seventh day, P < 0.05) and in CA3 (201% at seventh day, P < 0.05), but the total number of PDGFRß+ cells was not altered. As in controls, PDGFRß-immunoreactivity was detected in parenchymal NG2+ and GFAP+ cells. We also observed PDGFRß+ structural pericytes, detached reactive pericytes, and endothelial cells. After TBI, PDGFRß+ cells clustered in the perilesional cortex and thalamus, particularly during the first post-injury week. PDGFRß immunopositivity was observed in NG2+ and GFAP+ cells, structural pericytes, detached reactive pericytes, and endothelial cells. In some animals, PDGFRß vascular staining was observed around the cortical glial scar for up to 3 months. Our data revealed an acute accumulation of PDGFRß+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRß-signaling in blood vessel and post-injury tissue recovery. GLIA 2017;65:322-341.
[Mh] Termos MeSH primário: Astrócitos/classificação
Astrócitos/metabolismo
Lesões Encefálicas/patologia
Células Endoteliais/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos/metabolismo
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Pericitos/metabolismo
Pericitos/patologia
Proteoglicanas/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Glial Fibrillary Acidic Protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proteoglycans); 0 (chondroitin sulfate proteoglycan 4); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23094


  2 / 2091 MEDLINE  
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[PMID]:29374704
[Au] Autor:Cierpikowski P; Lis-Nawara A; Gajdzis P; Bar J
[Ad] Endereço:Department of Immunopathology and Molecular Biology, Wroclaw Medical University, Wroclaw, Poland cierpikowski@gmail.com.
[Ti] Título:PDGFRα/HER2 and PDGFRα/p53 Co-expression in Oral Squamous Cell Carcinoma.
[So] Source:Anticancer Res;38(2):795-802, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:AIM: The purpose of this study was to explore the parallel expression of platelet-derived growth factor receptor α (PDGFRα) and human epidermal growth factor receptor 2 (HER2) or p53 in relation to clinicopathological parameters of oral squamous cell carcinoma (OSCC) to define their role in progressive growth of tumor. MATERIALS AND METHODS: Expression of PDGFRα, HER2 and p53 was evaluated in 71 OSCC samples by immunohistochemistry. HER2 status was verified by fluorescence in situ hybridization. RESULTS: PDGFRα and p53 expression were associated with tumor grade (p=0.043 and p=0.040, respectively). HER2 expression was more frequent in advanced (III/IV) cancer (p=0.006). A positive correlation of PDGFRα with HER2 (r=0.267; p=0.024) and with p53 (r=0.266; p=0.025) was noted. PDGFRα/HER2 and PDGFRα/p53 co-expression was found more often in G3 than in G1 and G2 tumors (p=0.008 and p=0.015, respectively). CONCLUSION: Our study revealed that PDGFRα/HER2 and PDGFRα/p53 co-expression exists in poorly differentiated OSCCs, suggesting that cooperation between these proteins might enhance aggressive behavior of tumor.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Neoplasias de Cabeça e Pescoço/metabolismo
Neoplasias Bucais/metabolismo
Receptor ErbB-2/biossíntese
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/biossíntese
Proteína Supressora de Tumor p53/biossíntese
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/biossíntese
Carcinoma de Células Escamosas/patologia
Feminino
Neoplasias de Cabeça e Pescoço/patologia
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Neoplasias Bucais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  3 / 2091 MEDLINE  
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[PMID]:27777072
[Au] Autor:Bahlawane C; Schmitz M; Letellier E; Arumugam K; Nicot N; Nazarov PV; Haan S
[Ad] Endereço:Molecular Disease Mechanisms group, Life Sciences Research Unit, University of Luxembourg, Campus Belval, 6 Avenue du Swing, L-4367 Belvaux, Luxembourg. Electronic address: christelle.bahlawane@uni.lu.
[Ti] Título:Insights into ligand stimulation effects on gastro-intestinal stromal tumors signalling.
[So] Source:Cell Signal;29:138-149, 2017 01.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mutations in KIT or PDGFRA are responsible for >85% of gastrointestinal stromal tumors. The introduction of imatinib in the GIST therapy scheme revolutionized the patient outcome. Unfortunately, the therapy allows the disease stabilization instead of curation. Furthermore the resistance to the inhibitor arises in most cases within two first years of therapy. A thorough investigation of the signalling pathways activated by the major PDGFRA and KIT mutants encountered in the GIST landscape allowed to identify striking differences between the two receptor tyrosine kinases. PDGFRA mutants were not responsive to their ligand, PDGFAA, and displayed a high constitutive kinase activity. In contrast, all KIT mutants retained, in addition to their constitutive activation, the ability to be stimulated by their ligand. Kit mutants displayed a lower intrinsic kinase activity relative to PDGFRA mutants, while the KIT Exon 11 deletion mutant exhibited the highest intrinsic kinase activity among KIT mutants. At the transcriptomic level, the MAPK pathway was established as the most prominent activated pathway, which is commonly up-regulated by all PDGFRA and KIT mutants. Inhibition of this pathway, using the MEK inhibitor PD0325901, reduced the proliferation of GIST primary cells at nanomolar concentrations. Altogether, our data demonstrate the high value of MEK inhibitors for combination therapy in GIST treatment and more importantly the interest of evaluating the SCF expression profile in GIST patients presenting KIT mutations.
[Mh] Termos MeSH primário: Tumores do Estroma Gastrointestinal/metabolismo
Tumores do Estroma Gastrointestinal/patologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Linhagem Celular Tumoral
Tumores do Estroma Gastrointestinal/genética
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células HEK293
Seres Humanos
Ligantes
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Simulação de Dinâmica Molecular
Mutação/genética
Inibidores de Proteínas Quinases/farmacologia
Transporte Proteico
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Ligands); 0 (Protein Kinase Inhibitors); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  4 / 2091 MEDLINE  
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[PMID]:29206386
[Au] Autor:Lopez NE; Yeh JJ
[Ti] Título:Gastrointestinal Malignancy: Genetic Implications to Clinical Applications.
[So] Source:Cancer Treat Res;168:393-479, 2016.
[Is] ISSN:0927-3042
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alterations in the DNA sequences of genes, or mutations, have traditionally been viewed as the primary factors driving tumor progression, however, epigenetic evidence would suggest that some heritable traits are mediated by changes in DNA expression that are not dependent upon alterations in the primary DNA sequence. Advances in the genetic understanding of cancer have, in some instances, allowed for more precise administration of anti-neoplastic therapy. Targeted therapies, the aim of which are to target specific cellular proteins or processes used by the cancer cells, have been advocated to avoid the adverse side effects attributable to a lack of cell specificity associated with traditional chemotherapy. Here we aim to describe the current state of understanding regarding the genetic related causes of cancers, the targeted therapies aimed at killing them and the inter-relationship between these two.
[Mh] Termos MeSH primário: Neoplasias Gastrointestinais/genética
[Mh] Termos MeSH secundário: Quimioprevenção
Neoplasias Gastrointestinais/terapia
Tumores do Estroma Gastrointestinal/genética
Seres Humanos
Instabilidade de Microssatélites
Terapia de Alvo Molecular
Mutação
Proteínas Proto-Oncogênicas B-raf/genética
Proteínas Proto-Oncogênicas c-kit/genética
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Succinato Desidrogenase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 1.3.99.1 (Succinate Dehydrogenase); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


  5 / 2091 MEDLINE  
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[PMID]:29025601
[Au] Autor:Oberley MJ; Denton C; Ji J; Hiemenz M; Bhojwani D; Ostrow D; Wu S; Gaynon P; Raca G
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Children's Hospital Los Angeles, Los Angeles, California.
[Ti] Título:A neoplasm with FIP1L1-PDGFRA fusion presenting as pediatric T-cell lymphoblastic leukemia/lymphoma without eosinophilia.
[So] Source:Cancer Genet;216-217:91-99, 2017 Oct.
[Is] ISSN:2210-7762
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 2016 World Health Organization (2016 WHO) classification of hematopoietic malignancies classifies neoplasms with a fusion between the FIP1L1 and PDGFRA genes in 4q12 into a group called "myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB or FGFR1 or with PCM1-JAK2". Neoplasms characterized by this fusion are pluripotent stem cell disorders that can show both myeloid and lymphoid differentiation. They typically occur in adult patients and most are characterized by eosinophilia. We describe identification of a FIP1L1-PDGFRA fusion in a 13-year-old boy who presented with T-lymphoblastic leukemia/lymphoma without eosinophilia. Detection of FIP1L1-PDGFRA driven neoplasms at diagnosis is usually critical for proper treatment, since almost all reported cases responded to tyrosine kinase inhibitors. However, our patient's leukemia was refractory to standard chemotherapy, and did not show a meaningful response to tyrosine kinase inhibitor therapy. Testing for a FIP1L1-PDGFRA rearrangement is at present limited to patients with idiopathic hypereosinophilia, and we hypothesize that this abnormality may be under-diagnosed in children with acute leukemias.
[Mh] Termos MeSH primário: Eosinofilia/complicações
Proteínas de Fusão Oncogênicas/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/complicações
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Fatores de Poliadenilação e Clivagem de mRNA/genética
[Mh] Termos MeSH secundário: Adolescente
Criança
Cromossomos Humanos/genética
Genoma Humano
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Imuno-Histoquímica
Cariotipagem
Linfonodos/patologia
Masculino
Análise de Sequência com Séries de Oligonucleotídeos
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oncogene Proteins, Fusion); 0 (mRNA Cleavage and Polyadenylation Factors); EC 2.7.10.1 (FIP1L1-PDGFRA fusion protein, human); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[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:171014
[St] Status:MEDLINE


  6 / 2091 MEDLINE  
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[PMID]:29019285
[Au] Autor:Guru SA; Mir R; Bhat M; Najar I; Zuberi M; Sumi M; Masroor M; Gupta N; Saxena A
[Ad] Endereço:1 Maulana Azad Medical College, New Delhi, India.
[Ti] Título:PDGFRα promoter polymorphisms and expression patterns influence risk of development of imatinib-induced thrombocytopenia in chronic myeloid leukemia: A study from India.
[So] Source:Tumour Biol;39(10):1010428317713857, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor receptor has been implicated in many malignant and non-malignant diseases. Platelet-derived growth factor receptor-α is a tyrosine kinase and a side target for imatinib, a revolutionary drug for the treatment of chronic myeloid leukemia that has dramatically improved the survival of chronic myeloid leukemia patients. Given the importance of platelet-derived growth factor receptor in platelet development and its inhibition by imatinib, it was intriguing to analyze the role of platelet-derived growth factor receptor-α in relation to imatinib treatment in the development of imatinib-induced thrombocytopenia in chronic myeloid leukemia patients. We hypothesized that two known functional polymorphisms, +68GA insertion/deletion and -909C/A, in the promoter region of the platelet-derived growth factor receptor-α gene may affect the susceptibility of chronic myeloid leukemia patients receiving imatinib treatment to the development of thrombocytopenia. A case-control study was conducted among a cohort of chronic myeloid leukemia patients admitted to the Lok Nayak Hospital, New Delhi, India. A set of 100 patients of chronic myeloid leukemia in chronic phase and 100 age- and sex-matched healthy controls were studied. After initiation of imatinib treatment, the hematological response of chronic myeloid leukemia patients was monitored regularly for 2 years, in which the development of thrombocytopenia was the primary end point. Platelet-derived growth factor receptor-α promoter polymorphisms +68GA ins/del and -909C/A were studied by allele-specific polymerase chain reaction. Platelet-derived growth factor receptor-α messenger RNA expression was evaluated by quantitative real-time polymerase chain reaction. The messenger RNA expression results were expressed as 2 ± standard deviation. The distribution of +68GA ins/del promoter polymorphism genotypes differed significantly between the thrombocytopenic and non-thrombocytopenic chronic myeloid leukemia patient groups (p < 0.0001). Moreover, +68GA del/del and ins/del genotypes in imatinib-treated chronic myeloid leukemia patients were associated with an increased risk of developing thrombocytopenia, with odds ratios 6.5 (95% confidence interval = 2.02-0.89, p = 0.001) and 6.0 (95% confidence interval = 2.26-15.91, p = 0.0002), respectively. Similarly, -909C/A promoter polymorphism genotype distribution also differed significantly between thrombocytopenic and non-thrombocytopenic chronic myeloid leukemia patient groups (p = 0.02), and a significantly increased risk of imatinib-induced thrombocytopenia was associated with -909C/A polymorphism mutant homozygous (AA) genotypes the odds ratio being 7.7 (95% confidence interval 1.50 to 39.91, p = 0.009). However, no significant risk of imatinib-induced thrombocytopenia was found to be associated with heterozygous genotype (-909C/A) with odds ratio 1.9 (95% confidence interval = 0.86-4.56, p = 1.14). Platelet-derived growth factor receptor-α messenger RNA expression was significantly higher in chronic myeloid leukemia patients compared to controls (p = 0.008). Moreover, patients with imatinib-induced thrombocytopenia had a significantly lower platelet-derived growth factor receptor-α messenger RNA expression, compared to patients without thrombocytopenia (p = 0.01). A differential expression of platelet-derived growth factor receptor-α messenger RNA was observed with respect to different +68 GA ins/del and -909C/A polymorphism genotypes. The +68GA deletion allele and -909A allele were significantly associated with lower expression of platelet-derived growth factor receptor-α messenger RNA. The platelet-derived growth factor receptor-α +68GA del/del, +68GA ins/del, and -909AA genotypes are associated with an increased risk of developing thrombocytopenia in imatinib-treated chronic myeloid leukemia patients. A significantly lower platelet-derived growth factor receptor-α messenger RNA expression accompanies the +68GA deletion allele in an allele dose-dependent manner. Platelet-derived growth factor receptor-α -909AA genotype is also associated with lower expression of platelet-derived growth factor receptor-α. The downregulation of platelet-derived growth factor receptor-α expression may play a causative role in imatinib-induced thrombocytopenia, a common side effect, in the subset of chronic myeloid leukemia patients with platelet-derived growth factor receptor-α +68 GA ins/del, +68 GA del/del, and -909C/A genotypes.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Predisposição Genética para Doença/genética
Mesilato de Imatinib/efeitos adversos
Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Trombocitopenia/genética
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Feminino
Genótipo
Seres Humanos
Índia
Masculino
Meia-Idade
Reação em Cadeia da Polimerase
Polimorfismo de Nucleotídeo Único
Regiões Promotoras Genéticas/genética
Fatores de Risco
Trombocitopenia/induzido quimicamente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 8A1O1M485B (Imatinib Mesylate); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317713857


  7 / 2091 MEDLINE  
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[PMID]:28934221
[Au] Autor:Qian C; Wong CWY; Wu Z; He Q; Xia H; Tam PKH; Wong KKY; Lui VCH
[Ad] Endereço:Department of Surgery, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
[Ti] Título:Stage specific requirement of platelet-derived growth factor receptor-α in embryonic development.
[So] Source:PLoS One;12(9):e0184473, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Platelet-derived growth factor receptor alpha (PDGFRα) is a cell-surface receptor tyrosine kinase for platelet-derived growth factors. Correct timing and level of Pdgfra expression is crucial for embryo development, and deletion of Pdgfra caused developmental defects of multiple endoderm and mesoderm derived structures, resulting in a complex phenotypes including orofacial cleft, spina bifida, rib deformities, and omphalocele in mice. However, it is not clear if deletion of Pdgfra at different embryonic stages differentially affects these structures. PURPOSE: To address the temporal requirement of Pdgfra in embryonic development. METHODS: We have deleted the Pdgfra in Pdgfra-expressing tissues at different embryonic stages in mice, examined and quantified the developmental anomalies. RESULTS: Current study showed that (i) conditional deletion of Pdgfra at different embryonic days (between E7.5 and E10.5) resulted in orofacial cleft, spina bifida, rib cage deformities, and omphalocele, and (ii) the day of Pdgfra deletion influenced the combinations, incidence and severities of these anomalies. Deletion of Pdgfra caused apoptosis of Pdgfra-expressing tissues, and developmental defects of their derivatives. CONCLUSION: Orofacial cleft, spina bifida and omphalocele are among the commonest skeletal and abdominal wall defects of newborns, but their genetic etiologies are largely unknown. The remarkable resemblance of our conditional Pdgfra knockout embryos to theses human congenital anomalies, suggesting that dysregulated PDGFRA expression could cause these anomalies in human. Future work should aim at defining (a) the regulatory elements for the expression of the human PDGFRA during embryonic development, and (b) if mutations / sequence variations of these regulatory elements cause these anomalies.
[Mh] Termos MeSH primário: Desenvolvimento Embrionário/fisiologia
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Parede Abdominal/anormalidades
Parede Abdominal/embriologia
Anormalidades Múltiplas/embriologia
Anormalidades Múltiplas/genética
Anormalidades Múltiplas/metabolismo
Animais
Apoptose/fisiologia
Fenda Labial/embriologia
Fenda Labial/genética
Fenda Labial/metabolismo
Fissura Palatina/embriologia
Fissura Palatina/genética
Fissura Palatina/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Técnicas de Inativação de Genes
Hérnia Umbilical/embriologia
Hérnia Umbilical/genética
Hérnia Umbilical/metabolismo
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Esqueleto/anormalidades
Esqueleto/embriologia
Esqueleto/metabolismo
Disrafismo Espinal/embriologia
Disrafismo Espinal/genética
Disrafismo Espinal/metabolismo
Tamoxifeno
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
094ZI81Y45 (Tamoxifen); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184473


  8 / 2091 MEDLINE  
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[PMID]:28910446
[Au] Autor:Takahama S; Adetunji MO; Zhao T; Chen S; Li W; Tomarev SI
[Ad] Endereço:Section on Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Institutes of Health, Bethesda, Maryland, United States.
[Ti] Título:Retinal Astrocytes and GABAergic Wide-Field Amacrine Cells Express PDGFRα: Connection to Retinal Ganglion Cell Neuroprotection by PDGF-AA.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4703-4711, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Our previous experiments demonstrated that intravitreal injection of platelet-derived growth factor-AA (PDGF-AA) provides retinal ganglion cell (RGC) neuroprotection in a rodent model of glaucoma. Here we used PDGFRα-enhanced green fluorescent protein (EGFP) mice to identify retinal cells that may be essential for RGC protection by PDGF-AA. Methods: PDGFRα-EGFP mice expressing nuclear-targeted EGFP under the control of the PDGFRα promoter were used. Localization of PDGFRα in the neural retina was investigated by confocal imaging of EGFP fluorescence and immunofluorescent labeling with a panel of antibodies recognizing different retinal cell types. Primary cultures of mouse RGCs were produced by immunopanning. Neurobiotin injection of amacrine cells in a flat-mounted retina was used for the identification of EGFP-positive amacrine cells in the inner nuclear layer. Results: In the mouse neural retina, PDGFRα was preferentially localized in the ganglion cell and inner nuclear layers. Immunostaining of the retina demonstrated that astrocytes in the ganglion cell layer and a subpopulation of amacrine cells in the inner nuclear layer express PDGFRα, whereas RGCs (in vivo or in vitro) did not. PDGFRα-positive amacrine cells are likely to be Type 45 gamma-aminobutyric acidergic (GABAergic) wide-field amacrine cells. Conclusions: These data indicate that the neuroprotective effect of PDGF-AA in a rodent model of glaucoma could be mediated by astrocytes and/or a subpopulation of amacrine cells. We suggest that after intravitreal injection of PDGF-AA, these cells secrete factors protecting RGCs.
[Mh] Termos MeSH primário: Células Amácrinas/metabolismo
Astrócitos/metabolismo
Fator de Crescimento Derivado de Plaquetas/farmacologia
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
Células Ganglionares da Retina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Biotina/análogos & derivados
Biotina/farmacologia
Western Blotting
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Colina O-Acetiltransferase/metabolismo
Modelos Animais de Doenças
Proteínas de Fluorescência Verde/metabolismo
Camundongos
Camundongos Transgênicos
Microscopia Confocal
Microscopia de Fluorescência
Neuroproteção
Fármacos Neuroprotetores
Células Ganglionares da Retina/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Platelet-Derived Growth Factor); 0 (enhanced green fluorescent protein); 0 (neurobiotin); 0 (platelet-derived growth factor A); 147336-22-9 (Green Fluorescent Proteins); 56-12-2 (gamma-Aminobutyric Acid); 6SO6U10H04 (Biotin); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.21783


  9 / 2091 MEDLINE  
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[PMID]:28862476
[Au] Autor:Okuno SH; Maran A; Robinson SI
[Ad] Endereço:a Department of Oncology , Mayo Clinic , Rochester , MN USA.
[Ti] Título:Olaratumab for the treatment of advanced soft tissue sarcoma.
[So] Source:Expert Rev Anticancer Ther;17(10):883-887, 2017 Oct.
[Is] ISSN:1744-8328
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Olaratumab, a human monoclonal antibody against platelet derived growth factor receptor alpha (PDGFR- α), is the first drug that in combination with doxorubicin for the treatment of patients with advanced/metastatic soft tissue sarcoma (STS) that has showed an improved overall survival compared to doxorubicin alone. These initial results are exciting and have the potential to change the landscape of treatment for patients with STS. Areas covered: This article reviews the development of olaratumab for oncology use by reviewing articles in PubMed for 'platelet derived growth factor' and 'receptor' and 'soft tissue sarcoma'. We provide an overview of the published studies to date for olaratumab and specifically the use in soft tissue sarcoma. Expert commentary: Olaratumab is a well-tolerated drug that, when combined with doxorubicin, has shown an improved overall survival compared to doxorubicin alone and the phase III confirmatory study is eagerly awaited.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Sarcoma/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Doxorrubicina/administração & dosagem
Seres Humanos
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Sarcoma/patologia
Taxa de Sobrevida
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 80168379AG (Doxorubicin); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); TT6HN20MVF (olaratumab)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1080/14737140.2017.1374857


  10 / 2091 MEDLINE  
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[PMID]:28826084
[Au] Autor:Qin M; Tian Y; Sun X; Yu S; Xia J; Gong P; Zhang H; Zhao Y
[Ad] Endereço:Key Laboratory of Structure-Based Drug Design and Discovery (Shenyang Pharmaceutical University), Ministry of Education, 103 Wenhua Road, Shenyang 110016, PR China.
[Ti] Título:Novel methyl indolinone-6-carboxylates containing an indole moiety as angiokinase inhibitors.
[So] Source:Eur J Med Chem;139:492-502, 2017 Oct 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A novel series of methyl indolinone-6-carboxylates bearing an indole moiety were identified as potent angiokinase inhibitors. The most active compound, A8, potently targeted the kinase activities of vascular endothelial growth factor receptors 2 and 3, and platelet-derived growth factor receptors α and ß, with IC values in the nanomolar range. In addition, A8 effectively suppressed the proliferation of human umbilical vein endothelial cells, and HT-29 and MCF-7 cancer cells, by inducing apoptosis. Compound A8 is thus a promising candidate for further investigation.
[Mh] Termos MeSH primário: Ácidos Carboxílicos/farmacologia
Indóis/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Ácidos Carboxílicos/síntese química
Ácidos Carboxílicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Seres Humanos
Indóis/síntese química
Indóis/química
Estrutura Molecular
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/antagonistas & inibidores
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Relação Estrutura-Atividade
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
Receptor 3 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Receptor 3 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carboxylic Acids); 0 (Indoles); 0 (indolinone-6-carboxylate); EC 2.7.10.1 (FGFR1 protein, human); EC 2.7.10.1 (FLT4 protein, human); EC 2.7.10.1 (KDR protein, human); EC 2.7.10.1 (PDGFRB protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE



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