Base de dados : MEDLINE
Pesquisa : G05.360.340.024.340.375.500.791.560 [Categoria DeCS]
Referências encontradas : 38 [refinar]
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[PMID]:25940705
[Au] Autor:Wang M; Liu Y; Zou J; Yang R; Xuan F; Wang Y; Gao N; Cui H
[Ad] Endereço:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
[Ti] Título:Transcriptional co-activator TAZ sustains proliferation and tumorigenicity of neuroblastoma by targeting CTGF and PDGF-ß.
[So] Source:Oncotarget;6(11):9517-30, 2015 Apr 20.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma is a common childhood malignant tumor originated from the neural crest-derived sympathetic nervous system. A crucial event in the pathogenesis of neuroblastoma is to promote proliferation of neuroblasts, which is closely related to poor survival. However, mechanisms for regulation of cell proliferation and tumorigenicity in neuroblastoma are not well understood. Here, we report that overexpression of TAZ in neuroblastoma BE(2)-C cells causes increases in cell proliferation, self renewal and colony formation, which was restored back to its original levels by knockdown of TAZ in TAZ-overexpression cells. Inhibition of endogenous TAZ attenuated cell proliferation, colony formation and tumor development in neuroblastoma SK-N-AS cell, which could be rescued by re-introduction of TAZ into TAZ-knockdown cells. In addition, we found that overexpressing TAZ-mediated induction of CTGF and PDGF-ß expression, cell proliferation and colony formation were inhibited by knocking down CTGF and PDGF-ß with siRNA in TAZ-overexpressing cell. Overall, our findings suggested that TAZ plays an essential role in regulating cell proliferation and tumorigenesis in neuroblastoma cells. Thus, TAZ seems to be a novel and promising target for the treatment of neuroblastoma.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Peptídeos e Proteínas de Sinalização Intracelular/fisiologia
Proteínas de Neoplasias/fisiologia
Neuroblastoma/patologia
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Divisão Celular
Linhagem Celular Tumoral
Fator de Crescimento do Tecido Conjuntivo/antagonistas & inibidores
Fator de Crescimento do Tecido Conjuntivo/biossíntese
Fator de Crescimento do Tecido Conjuntivo/genética
Genes sis
Xenoenxertos
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/antagonistas & inibidores
Peptídeos e Proteínas de Sinalização Intracelular/biossíntese
Peptídeos e Proteínas de Sinalização Intracelular/genética
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Terapia de Alvo Molecular
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/biossíntese
Proteínas de Neoplasias/genética
Neuroblastoma/genética
Prognóstico
Proteínas Proto-Oncogênicas c-sis/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-sis/biossíntese
Interferência de RNA
RNA Interferente Pequeno/genética
Proteínas Recombinantes de Fusão/metabolismo
Taxa de Sobrevida
Transfecção
Ensaio Tumoral de Célula-Tronco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTGF protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (Neoplasm Proteins); 0 (Proto-Oncogene Proteins c-sis); 0 (RNA, Small Interfering); 0 (Recombinant Fusion Proteins); 0 (WWTR1 protein, human); 139568-91-5 (Connective Tissue Growth Factor)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150506
[St] Status:MEDLINE


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[PMID]:25832657
[Au] Autor:Keogh MJ; Pyle A; Daud D; Griffin H; Douroudis K; Eglon G; Miller J; Horvath R; Chinnery PF
[Ad] Endereço:From the Wellcome Centre for Mitochondrial Research (M.J.K., A.P., D.D., H.G., K.D., G.E., R.H., P.F.C.), Institute of Genetic Medicine, Centre for Life, Newcastle University; and Royal Victoria Infirmary (M.J.K., J.M., R.H., P.F.C.), Newcastle Upon Tyne, UK.
[Ti] Título:Clinical heterogeneity of primary familial brain calcification due to a novel mutation in PDGFB.
[So] Source:Neurology;84(17):1818-20, 2015 Apr 28.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doenças dos Gânglios da Base/fisiopatologia
Calcinose/fisiopatologia
Genes sis/genética
[Mh] Termos MeSH secundário: Adulto
Doenças dos Gânglios da Base/genética
Doenças dos Gânglios da Base/patologia
Calcinose/genética
Calcinose/patologia
Feminino
Seres Humanos
Meia-Idade
Fenótipo
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1507
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150403
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000001517


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[PMID]:24973215
[Au] Autor:Saeed AA; Genové G; Li T; Lütjohann D; Olin M; Mast N; Pikuleva IA; Crick P; Wang Y; Griffiths W; Betsholtz C; Björkhem I
[Ad] Endereço:From the Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska University Hospital, Karolinska Institute, Huddinge, Stockholm 141 86, Sweden, the Department of Biochemistry, Faculty of Medicine, University of Khartoum, 11111 Khartoum, Sudan.
[Ti] Título:Effects of a disrupted blood-brain barrier on cholesterol homeostasis in the brain.
[So] Source:J Biol Chem;289(34):23712-22, 2014 Aug 22.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The presence of the blood-brain barrier (BBB) is critical for cholesterol metabolism in the brain, preventing uptake of lipoprotein-bound cholesterol from the circulation. The metabolic consequences of a leaking BBB for cholesterol metabolism have not been studied previously. Here we used a pericyte-deficient mouse model, Pdgfb(ret/ret), shown to have increased permeability of the BBB to a range of low-molecular mass and high-molecular mass tracers. There was a significant accumulation of plant sterols in the brains of the Pdgfb(ret/ret) mice. By dietary treatment with 0.3% deuterium-labeled cholesterol, we could demonstrate a significant flux of cholesterol from the circulation into the brains of the mutant mice roughly corresponding to about half of the measured turnover of cholesterol in the brain. We expected the cholesterol flux into the brain to cause a down-regulation of cholesterol synthesis. Instead, cholesterol synthesis was increased by about 60%. The levels of 24(S)-hydroxycholesterol (24S-OHC) were significantly reduced in the brains of the pericyte-deficient mice but increased in the circulation. After treatment with 1% cholesterol in diet, the difference in cholesterol synthesis between mutants and controls disappeared. The findings are consistent with increased leakage of 24S-OHC from the brain into the circulation in the pericyte-deficient mice. This oxysterol is an efficient suppressor of cholesterol synthesis, and the results are consistent with a regulatory role of 24S-OHC in the brain. To our knowledge, this is the first demonstration that a defective BBB may lead to increased flux of a lipophilic compound out from the brain. The relevance of the findings for the human situation is discussed.
[Mh] Termos MeSH primário: Barreira Hematoencefálica
Encéfalo/metabolismo
Colesterol/metabolismo
Homeostase
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Colesterol/biossíntese
Primers do DNA
Genes sis
Homeostase/genética
Camundongos
Camundongos Transgênicos
Plantas/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Esteróis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Primers); 0 (Sterols); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140629
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M114.556159


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[PMID]:24929166
[Au] Autor:Scharpfenecker M; Floot B; Russell NS; Coppes RP; Stewart FA
[Ad] Endereço:Division of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands. Electronic address: m.scharpfenecker@nki.nl.
[Ti] Título:Thalidomide ameliorates inflammation and vascular injury but aggravates tubular damage in the irradiated mouse kidney.
[So] Source:Int J Radiat Oncol Biol Phys;89(3):599-606, 2014 Jul 01.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The late side effects of kidney irradiation include vascular damage and fibrosis, which are promoted by an irradiation-induced inflammatory response. We therefore treated kidney-irradiated mice with the anti-inflammatory and angiogenesis-modulating drug thalidomide in an attempt to prevent the development of late normal tissue damage and radiation nephropathy in the mouse kidney. METHODS AND MATERIALS: Kidneys of C57Bl/6 mice were irradiated with a single dose of 14 Gy. Starting from week 16 after irradiation, the mice were fed with thalidomide-containing chow (100 mg/kg body weight/day). Gene expression and kidney histology were analyzed at 40 weeks and blood samples at 10, 20, 30, and 40 weeks after irradiation. RESULTS: Thalidomide improved the vascular structure and vessel perfusion after irradiation, associated with a normalization of pericyte coverage. The drug also reduced infiltration of inflammatory cells but could not suppress the development of fibrosis. Irradiation-induced changes in hematocrit and blood urea nitrogen levels were not rescued by thalidomide. Moreover, thalidomide worsened tubular damage after irradiation and also negatively affected basal tubular function. CONCLUSIONS: Thalidomide improved the inflammatory and vascular side effects of kidney irradiation but could not reverse tubular toxicity, which probably prevented preservation of kidney function.
[Mh] Termos MeSH primário: Moduladores da Angiogênese/farmacologia
Anti-Inflamatórios/farmacologia
Túbulos Renais/efeitos dos fármacos
Rim/efeitos da radiação
Lesões Experimentais por Radiação/prevenção & controle
Talidomida/farmacologia
[Mh] Termos MeSH secundário: Moduladores da Angiogênese/efeitos adversos
Animais
Anti-Inflamatórios/efeitos adversos
Feminino
Fibrose
Genes sis/efeitos dos fármacos
Taxa de Filtração Glomerular/efeitos dos fármacos
Taxa de Filtração Glomerular/efeitos da radiação
Rim/irrigação sanguínea
Rim/efeitos dos fármacos
Rim/patologia
Túbulos Renais/efeitos da radiação
Camundongos
Camundongos Endogâmicos C57BL
Nefrite/patologia
Nefrite/prevenção & controle
Talidomida/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiogenesis Modulating Agents); 0 (Anti-Inflammatory Agents); 4Z8R6ORS6L (Thalidomide)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:140615
[Lr] Data última revisão:
140615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140615
[St] Status:MEDLINE


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[PMID]:23912956
[Au] Autor:Slattery ML; John EM; Stern MC; Herrick J; Lundgreen A; Giuliano AR; Hines L; Baumgartner KB; Torres-Mejia G; Wolff RK
[Ad] Endereço:Department of Medicine, University of Utah, 383 Colorow, Salt Lake City, UT 84108, USA. marty.slattery@hsc.utah.edu
[Ti] Título:Associations with growth factor genes (FGF1, FGF2, PDGFB, FGFR2, NRG2, EGF, ERBB2) with breast cancer risk and survival: the Breast Cancer Health Disparities Study.
[So] Source:Breast Cancer Res Treat;140(3):587-601, 2013 Aug.
[Is] ISSN:1573-7217
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Growth factors (GF) stimulate cell proliferation through binding to cell membrane receptors and are thought to be involved in cancer risk and survival. We examined how genetic variation in epidermal growth factor (EGF), neuregulin 2 (NRG2), ERBB2 (HER2/neu), fibroblast growth factors 1 and 2 (FGF1 and FGF2) and its receptor 2 (FGFR2), and platelet-derived growth factor B (PDGFB) independently and collectively influence breast cancer risk and survival. We analyzed data from the Breast Cancer Health Disparities Study which includes Hispanic (2,111 cases, 2,597 controls) and non-Hispanic white (1,481 cases, 1,586 controls) women. Adaptive rank-truncated product (ARTP) analysis was conducted to determine gene significance. Odds ratios (OR) and 95 % confidence intervals were obtained from conditional logistic regression models to estimate breast cancer risk and Cox proportional hazard models were used to estimate hazard ratios (HR) of dying from breast cancer. We assessed Native American (NA) ancestry using 104 ancestry informative markers. We observed few significant associations with breast cancer risk overall or by menopausal status other than for FGFR2 rs2981582. This SNP was significantly associated with ER+/PR+ (OR 1.66, 95 % CI 1.37-2.00) and ER+/PR- (OR 1.54, 95 % CI 1.03-2.31) tumors. Multiple SNPs in FGF1, FGF2, and NRG2 significantly interacted with multiple SNPs in EGFR, ERBB2, FGFR2, and PDGFB, suggesting that breast cancer risk is dependent on the collective effects of genetic variants in other GFs. Both FGF1 and ERBB2 significantly influenced overall survival, especially among women with low levels of NA ancestry (P ARTP = 0.007 and 0.003, respectively). Our findings suggest that genetic variants in growth factors signaling appear to influence breast cancer risk through their combined effects. Genetic variation in ERBB2 and FGF1 appear to be associated with survival after diagnosis with breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias da Mama/mortalidade
Peptídeos e Proteínas de Sinalização Intercelular/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Fator de Crescimento Epidérmico/genética
Grupo com Ancestrais do Continente Europeu/genética
Feminino
Fator 1 de Crescimento de Fibroblastos/genética
Fator 2 de Crescimento de Fibroblastos/genética
Genes erbB-2
Genes sis
Hispano-Americanos/genética
Seres Humanos
Índios Norte-Americanos/genética
Meia-Idade
Fatores de Crescimento Neural/genética
Polimorfismo de Nucleotídeo Único
Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Intercellular Signaling Peptides and Proteins); 0 (NRG2 protein, human); 0 (Nerve Growth Factors); 103107-01-3 (Fibroblast Growth Factor 2); 104781-85-3 (Fibroblast Growth Factor 1); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (FGFR2 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130806
[St] Status:MEDLINE
[do] DOI:10.1007/s10549-013-2644-5


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[PMID]:23614918
[Au] Autor:Ishigami T; Hida Y; Matsudate Y; Murao K; Kubo Y
[Ad] Endereço:Department of Dermatology, Institute of Health Biosciences, the University of Tokushima Graduate School, Tokushima, Japan.
[Ti] Título:The involvement of fibroblast growth factor receptor signaling pathways in dermatofibroma and dermatofibrosarcoma protuberans.
[So] Source:J Med Invest;60(1-2):106-13, 2013.
[Is] ISSN:1349-6867
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Fibroblast growth factors (FGFs) and their receptors (FGFRs) control a wide range of biological functions; however, their involvement in the pathogenesis of dermatofibroma (DF) and dermatofibrosarcoma protuberans (DFSP) is currently unknown. In this study, we first confirmed the histological diagnosis by detecting fusion COL1A1-PDGFB transcripts in DFSP, and examined the expression of all FGFRs (FGFR1-4), some of their ligands (FGF1, 2, 9), and forkhead box N1 (FOXN1) as a downstream target of FGFR3 in DF and DFSP by immunohistochemical analysis. Although we failed to detect the expression of FGF1 and FGF9 as specific ligands for FGFR3 in DF, overexpression of FGFR3 and FOXN1 was observed in the epidermal regions of DF, suggesting that the epidermal regions of DF were similar to seborrhoeic keratosis both in terms of histological features and the activation of FGFR3/FOXN1. In addition, strong expression of FGF2 and FGFR4 was observed in the tumor lesions of DF. Expression patterns of FGFR3/FOXN1 and FGF2/FGFR4 in DF were in contrast with those of DFSP. The activation of FGFR signaling pathways may be not only relevant to the pathogenesis of DF, but also very useful in the differential diagnosis of DF and DFSP.
[Mh] Termos MeSH primário: Dermatofibrossarcoma/etiologia
Histiocitoma Fibroso Benigno/etiologia
Receptores de Fatores de Crescimento de Fibroblastos/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Colágeno Tipo I/genética
Dermatofibrossarcoma/metabolismo
Feminino
Fatores de Transcrição Forkhead/análise
Genes sis
Histiocitoma Fibroso Benigno/metabolismo
Seres Humanos
Masculino
Meia-Idade
Receptores de Fatores de Crescimento de Fibroblastos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Forkhead Transcription Factors); 0 (Receptors, Fibroblast Growth Factor); 0 (Whn protein); 0 (collagen type I, alpha 1 chain)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130426
[St] Status:MEDLINE


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[PMID]:23537647
[Au] Autor:Zhang Y; Zhao Y; Li L; Shen Y; Cai X; Zhang X; Ye L
[Ad] Endereço:Department of Biochemistry, College of Life Sciences, Nankai University, Tianjin 300071, China.
[Ti] Título:The oncoprotein HBXIP upregulates PDGFB via activating transcription factor Sp1 to promote the proliferation of breast cancer cells.
[So] Source:Biochem Biophys Res Commun;434(2):305-10, 2013 May 03.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have reported that the oncoprotein hepatitis B virus X-interacting protein (HBXIP) acts as a novel transcriptional coactivator to promote proliferation and migration of breast cancer cells. Previously, we showed that HBXIP was able to activate nuclear factor-κB (NF-κB) in breast cancer cells. As an oncogene, the platelet-derived growth factor beta polypeptide (PDGFB) plays crucial roles in carcinogenesis. In the present study, we found that both HBXIP and PDGFB were highly expressed in breast cancer cell lines. Interestingly, HBXIP was able to increase transcriptional activity of NF-κB through PDGFB, suggesting that HBXIP is associated with PDGFB in the cells. Moreover, HBXIP was able to upregulate PDGFB at the levels of mRNA, protein and promoter in the cells. Then, we identified that HBXIP stimulated the promoter of PDGFB through activating transcription factor Sp1. In function, HBXIP enhanced the proliferation of breast cancer cells through PDGFB in vitro. Thus, we conclude that HBXIP upregulates PDGFB via activating transcription factor Sp1 to promote proliferation of breast cancer cells.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Neoplasias da Mama/patologia
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Genes sis
Fator de Transcrição Sp1/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Neoplasias da Mama/metabolismo
Imunoprecipitação da Cromatina
Clonagem Molecular
Feminino
Genes Reporter
Seres Humanos
Luciferases/genética
Luciferases/metabolismo
Células MCF-7
Proteínas Oncogênicas/genética
Proteínas Oncogênicas/metabolismo
Plasmídeos/genética
Plasmídeos/metabolismo
Regiões Promotoras Genéticas
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Fator de Transcrição Sp1/genética
Ativação Transcricional
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (HBXIP protein, human); 0 (Oncogene Proteins); 0 (RNA, Small Interfering); 0 (Sp1 Transcription Factor); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:130506
[Lr] Data última revisão:
130506
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130330
[St] Status:MEDLINE


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[PMID]:23207290
[Au] Autor:Walluks K; Chen Y; Woelfel C; Yang L; Cui T; Seliger C; Geier C; Knösel T; Hauke S; Petersen I
[Ad] Endereço:Institute of Pathology, Jena University Hospital, Friedrich-Schiller-University Jena, Ziegelmühlenweg 1, Jena, Germany.
[Ti] Título:Molecular and clinicopathological analysis of dermatofibrosarcoma protuberans.
[So] Source:Pathol Res Pract;209(1):30-5, 2013 Jan 15.
[Is] ISSN:1618-0631
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Dermatofibrosarcoma protuberans (DFSP) is a dermal and subcutaneous tumor of intermediate malignancy. The most remarkable cytogenetic feature of DFSP is the chromosomal translocation t(17;22)(q22;q13), causing a fusion of the platelet-derived growth factor beta chain (PDGFB) gene at 22q13, and the collagen type 1 alpha 1 (COL1A1) at 17q22. The aim of the study was to analyze the molecular characteristic of DFSP in conjunction with histopathological and clinical features. We performed fluorescence in situ hybridization (FISH) and multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) to detect chromosomal translocations and fusion gene transcripts in 16 formalin-fixed, paraffin-embedded DFSP samples. In addition, the amplification of PDGFB was also evaluated in the 16 DFSP samples by real-time PCR. FISH analysis revealed that all the 16 samples exhibited COL1A1-PDGFB gene fusion. Eleven out of 11 informative cases (100%) showed fusion transcripts by multiplex RT-PCR analysis. Various exons of the COL1A1 gene were fused with the PDGFB gene. Among them, exon 25 was found to be more frequently involved. Real-time PCR showed that the PDGFB copy number increase in the DFSP samples was higher than in normal skin tissues (p=0.007). Values of FISH fusion signals and PDGFB DNA analysis were variable between samples, but suggested that increased values might be associated with parameters of tumor progression. Our results confirm that analysis of the COL1A1-PDGFB status by FISH and RT-PCR is a useful tool in the confirmation of a DFSP diagnosis. In addition, the analysis of PDGFB copy number status may become a useful diagnostic marker since the gene is a potential target for treatment of DFSP patients.
[Mh] Termos MeSH primário: Colágeno Tipo I/genética
Dermatofibrossarcoma/genética
Genes sis/genética
Proteínas de Fusão Oncogênicas/genética
[Mh] Termos MeSH secundário: Adulto
Idoso de 80 Anos ou mais
Feminino
Amplificação de Genes
Seres Humanos
Hibridização in Situ Fluorescente
Masculino
Meia-Idade
Reação em Cadeia da Polimerase Multiplex
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Oncogene Proteins, Fusion); 0 (collagen type I, alpha 1 chain)
[Em] Mês de entrada:1307
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121205
[St] Status:MEDLINE


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[PMID]:22345562
[Au] Autor:Holmes KM; Annala M; Chua CY; Dunlap SM; Liu Y; Hugen N; Moore LM; Cogdell D; Hu L; Nykter M; Hess K; Fuller GN; Zhang W
[Ad] Endereço:Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
[Ti] Título:Insulin-like growth factor-binding protein 2-driven glioma progression is prevented by blocking a clinically significant integrin, integrin-linked kinase, and NF-κB network.
[So] Source:Proc Natl Acad Sci U S A;109(9):3475-80, 2012 Feb 28.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Insulin-like growth factor-binding protein 2 (IGFBP2) is increasingly recognized as a glioma oncogene, emerging as a target for therapeutic intervention. In this study, we used an integrative approach to characterizing the IGFBP2 network, combining transcriptional profiling of human glioma with validation in glial cells and the replication-competent ASLV long terminal repeat with a splice acceptor/tv-a glioma mouse system. We demonstrated that IGFBP2 expression is closely linked to genes in the integrin and integrin-linked kinase (ILK) pathways and that these genes are associated with prognosis. We further showed that IGFBP2 activates integrin ß1 and downstream invasion pathways, requires ILK to induce cell motility, and activates NF-κB. Most significantly, the IGFBP2/integrin/ILK/NF-κB network functions as a physiologically active signaling pathway in vivo by driving glioma progression; interfering with any point in the pathway markedly inhibits progression. The results of this study reveal a signaling pathway that is both targetable and highly relevant to improving the survival of glioma patients.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia
Terapia Genética
Vetores Genéticos/uso terapêutico
Glioblastoma/patologia
Proteína 2 de Ligação a Fator de Crescimento Semelhante à Insulina/fisiologia
Integrina beta1/fisiologia
NF-kappa B/fisiologia
Proteínas de Neoplasias/fisiologia
Proteínas Serina-Treonina Quinases/fisiologia
[Mh] Termos MeSH secundário: Animais
Astrocitoma/genética
Astrocitoma/metabolismo
Proteínas Aviárias/genética
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/terapia
Linhagem Celular Tumoral
Progressão da Doença
Regulação Neoplásica da Expressão Gênica
Genes Sintéticos
Genes sis
Vetores Genéticos/administração & dosagem
Glioblastoma/genética
Glioblastoma/terapia
Seres Humanos
Proteínas I-kappa B/genética
Proteínas I-kappa B/toxicidade
Proteína 2 de Ligação a Fator de Crescimento Semelhante à Insulina/biossíntese
Proteína 2 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Proteína 2 de Ligação a Fator de Crescimento Semelhante à Insulina/toxicidade
Proteínas de Filamentos Intermediários/genética
Estimativa de Kaplan-Meier
Camundongos
Camundongos Transgênicos
Inibidor de NF-kappaB alfa
Invasividade Neoplásica
Proteínas de Neoplasias/biossíntese
Proteínas de Neoplasias/genética
Proteínas do Tecido Nervoso/genética
Nestina
Oligodendroglioma/genética
Oligodendroglioma/metabolismo
Prognóstico
Proteínas Serina-Treonina Quinases/toxicidade
Receptores Virais/genética
Retroviridae
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Avian Proteins); 0 (I-kappa B Proteins); 0 (Insulin-Like Growth Factor Binding Protein 2); 0 (Integrin beta1); 0 (Intermediate Filament Proteins); 0 (NES protein, human); 0 (NF-kappa B); 0 (NFKBIA protein, human); 0 (Neoplasm Proteins); 0 (Nerve Tissue Proteins); 0 (Nes protein, mouse); 0 (Nestin); 0 (Nfkbia protein, mouse); 0 (Receptors, Virus); 0 (Tva receptor); 139874-52-5 (NF-KappaB Inhibitor alpha); EC 2.7.1.- (integrin-linked kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120221
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1120375109


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[PMID]:20468047
[Au] Autor:Masui K; Suzuki SO; Torisu R; Goldman JE; Canoll P; Iwaki T
[Ad] Endereço:Department of Neuropathology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
[Ti] Título:Glial progenitors in the brainstem give rise to malignant gliomas by platelet-derived growth factor stimulation.
[So] Source:Glia;58(9):1050-65, 2010 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glial progenitors in the white matter and the subventricular zone are the major population of cycling cells in the postnatal central nervous system, and thought to be candidates for glioma-initiating cells. However, less is known about the dividing cell populations in the brainstem than those in the cerebrum, leading to the lag of basic understanding of brainstem gliomas. We herein demonstrate much fewer cycling glial progenitors exist in the brainstem than in the cerebrum. We also show that infecting brainstem glial progenitors with PDGFB-green fluorescent protein (GFP)-expressing retrovirus induced tumors that closely resembled human malignant gliomas. Of note, brainstem tumors grew more slowly than cerebral tumors induced by the same retrovirus, and >80% tumor cells in the brainstem consisted of GFP-positive, infected progenitors while GFP-positive cells in the cerebral tumors were <20%. These indicate that cerebral tumors progressed rapidly by recruiting resident progenitors via paracrine mechanism whereas brainstem tumors grew more slowly by clonal expansion of the infected population. The cerebral and brainstem glial progenitors similarly showed reversible dedifferentiation upon PDGF stimulation in vitro and did not show the intrinsic difference in terms of the responsiveness to PDGF. We therefore suggest that slower, monoclonal progression pattern of the brainstem tumors is at least partly due to the environmental factors including the cell density of the glial progenitors. Together, these findings are the first implications regarding the cell-of-origin and the gliomagenesis in the brainstem.
[Mh] Termos MeSH primário: Neoplasias do Tronco Encefálico/fisiopatologia
Tronco Encefálico/fisiopatologia
Glioma/fisiopatologia
Neuroglia/fisiologia
Fator de Crescimento Derivado de Plaquetas/metabolismo
Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/fisiopatologia
Tronco Encefálico/patologia
Neoplasias do Tronco Encefálico/patologia
Diferenciação Celular
Células Cultivadas
Cerebelo/fisiologia
Criança
Feminino
Genes sis
Vetores Genéticos
Glioma/patologia
Proteínas de Fluorescência Verde/genética
Seres Humanos
Masculino
Fator de Crescimento Derivado de Plaquetas/genética
Ratos
Retroviridae
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet-Derived Growth Factor); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1008
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100515
[St] Status:MEDLINE
[do] DOI:10.1002/glia.20986



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