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Pesquisa : D08.811.913.696.620.682.700.559.842.249 [Categoria DeCS]
Referências encontradas : 150 [refinar]
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  1 / 150 MEDLINE  
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[PMID]:26995975
[Au] Autor:Kit OI; Vodolazhsky DL; Timoshkina NN; Przhedetsky YV; Khokhlova OV
[Ti] Título:[Molecular biology of familial cases of human melanoma].
[So] Source:Vopr Onkol;61(6):889-97, 2015.
[Is] ISSN:0507-3758
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Skin melanoma is an etiologically heterogeneous disease, the development of which is related to a complex interaction of environmental factors and individual genetic characteristics. This article provides current molecular-genetic aspects of familial cases of melanoma and polymorphism of genes directly related to the risk of developing this hereditary disease. The studies of hereditary cancer cases add our knowledge of mechanisms oncotransformation, genetic changes in signaling pathways, which are responsible for invasiveness, metastasis and drug resistance of melanoma cells of the skin.
[Mh] Termos MeSH primário: Quinase 4 Dependente de Ciclina/genética
Interação Gene-Ambiente
Genes p16
Melanoma/genética
Fator de Transcrição Associado à Microftalmia/genética
Mutação
Receptor Tipo 1 de Melanocortina/genética
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Melanoma/etiologia
Proteínas Oncogênicas v-raf/genética
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias Cutâneas/etiologia
Xeroderma Pigmentoso/genética
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MITF protein, human); 0 (Microphthalmia-Associated Transcription Factor); 0 (Receptor, Melanocortin, Type 1); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:160321
[Lr] Data última revisão:
160321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160322
[St] Status:MEDLINE


  2 / 150 MEDLINE  
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[PMID]:25859961
[Au] Autor:Vikis HG; Guan KL
[Ad] Endereço:Department of Pharmacology & Toxicology, MCW Cancer Center, Medical College of Wisconsin, Milwaukee, WI, 53202, USA, hvikis@gmail.com.
[Ti] Título:Glutathione-S-transferase (GST)-fusion based assays for studying protein-protein interactions.
[So] Source:Methods Mol Biol;1278:353-64, 2015.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glutathione-S-transferase (GST)-fusion proteins have become an effective reagent to use in the study of protein-protein interactions. GST-fusion proteins can be produced in bacterial and mammalian cells in large quantities and purified rapidly. GST can be coupled to a glutathione matrix, which permits its use as an effective affinity column to study interactions in vitro or to purify protein complexes in cells expressing the GST-fusion protein. Here, we provide a technical description of the utilization of GST-fusion proteins as both a tool to study protein-protein interactions and also as a means to purify interacting proteins.
[Mh] Termos MeSH primário: Proteínas Oncogênicas v-raf/química
Mapeamento de Interação de Proteínas/métodos
Mapas de Interação de Proteínas
Proteínas ras/química
[Mh] Termos MeSH secundário: Anticorpos/química
Anticorpos/imunologia
Sítios de Ligação
Cromatografia de Afinidade
Glutationa Transferase/química
Glutationa Transferase/imunologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies); EC 2.5.1.18 (Glutathione Transferase); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:150411
[Lr] Data última revisão:
150411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150411
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-2425-7_22


  3 / 150 MEDLINE  
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[PMID]:25556681
[Au] Autor:Katsuya Y; Yoshida A; Watanabe S; Tsuta K
[Ad] Endereço:Division of Pathology and Clinical Laboratory, National Cancer Centre Hospital, Tokyo, Japan.
[Ti] Título:Tumour-to-tumour metastasis from papillary thyroid carcinoma with BRAF mutation to lung adenocarcinoma with EGFR mutation: the utility of mutation-specific antibodies.
[So] Source:Histopathology;67(2):262-6, 2015 Aug.
[Is] ISSN:1365-2559
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: Tumour-to-tumour metastasis is a rare event. The aim of this study is to demonstrate the utility of mutation-specific antibodies to prove the occurrence of metastatic papillary thyroid cancer donor into lung adenocarcinoma recipient. METHODS AND RESULTS: We report the case of an 80-year-old woman who had a papillary thyroid carcinoma with a v-raf murine sarcoma viral oncogene homologue B1 mutation that metastasized into a lung adenocarcinoma with an epidermal growth factor receptor mutation. Immunohistochemical analysis with mutation-specific antibodies not only clearly revealed two components, but also revealed their gene mutation statuses. CONCLUSIONS: As a component of multimodal diagnostic tools, immunohistochemistry can avoid some pitfalls involved in the molecular diagnosis of complicated cases (such as our own) and can help to ensure that patients receive optimal treatments.
[Mh] Termos MeSH primário: Adenocarcinoma/diagnóstico
Carcinoma/diagnóstico
Neoplasias Pulmonares/diagnóstico
Segunda Neoplasia Primária
Proteínas Proto-Oncogênicas B-raf/genética
Receptor do Fator de Crescimento Epidérmico/genética
Neoplasias da Glândula Tireoide/diagnóstico
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Idoso de 80 Anos ou mais
Carcinoma/genética
Carcinoma Papilar
Análise Mutacional de DNA
Feminino
Seres Humanos
Neoplasias Pulmonares/genética
Proteínas Oncogênicas v-raf/genética
Neoplasias da Glândula Tireoide/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150106
[St] Status:MEDLINE
[do] DOI:10.1111/his.12643


  4 / 150 MEDLINE  
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[PMID]:22786759
[Au] Autor:Miranda E; Bianchi P; Destro A; Morenghi E; Malesci A; Santoro A; Laghi L; Roncalli M
[Ad] Endereço:Molecular Genetics Laboratory, Humanitas Clinical and Research Center, Milan, Italy.
[Ti] Título:Genetic and epigenetic alterations in primary colorectal cancers and related lymph node and liver metastases.
[So] Source:Cancer;119(2):266-76, 2013 Jan 15.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Colorectal cancer (CRC) prognosis and survival are strictly related to the development of distant metastases. New targeted therapies have increased patient survival, but the objective response rate is still very limited, partially because of a traditional focus on designing treatment according to the molecular profile of the primary tumor regardless the diversity between the primary tumor and metastases. The objective of this study was to evaluate the presence of molecular heterogeneity during metastatic progression and its potential impact on clinical treatment. METHODS: The authors analyzed v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) codon 12 mutations, the v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) thymine to adenine substitution at codon 1788, and tumor protein 53 (p53) mutations and investigated promoter methylation of Ras association (RalGDS/AF-6) domain family member 1 protein (RASSF1a), E-cadherin, and cyclin-dependent kinase inhibitor 2A (p16INK4a) in 101 primary CRCs (67 stage III and 34 stage IV) and related lymph node and liver metastases. RESULTS: Lymph node metastases were characterized by fewer alterations compared with primary tumors and liver metastases, especially KRAS (P = .03) and p16INK4a (P = .05). Genetic changes, when detectable in metastases, mostly were retained from the primary tumor, whereas epigenetic changes more frequently were acquired de novo. Overall, 31 distinct CRC molecular profiles were detected, none of which characterized a particular tumor stage. When the metastatic lesions also were included in the profiles, there were 53 distinct molecular profiles in 67 patients with stage III disease and 34 distinct molecular profiles in 34 patients with stage IV disease. CONCLUSIONS: Lymph node and liver metastases appear to originate in clonally different processes, with more molecular alterations occurring in distant metastases than in lymph node metastases and with elevated heterogeneity of the primary tumor. Thus, potential prognostic targets should be carefully evaluated for their heterogeneity in both primary tumors and distant metastases to avoid erroneous misclassification.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Epigênese Genética
Neoplasias Hepáticas/genética
Mutação
[Mh] Termos MeSH secundário: Caderinas/genética
Neoplasias Colorretais/patologia
Inibidor p16 de Quinase Dependente de Ciclina/genética
Metilação de DNA
Análise Mutacional de DNA
Seres Humanos
Neoplasias Hepáticas/secundário
Metástase Linfática
Estadiamento de Neoplasias
Proteínas Oncogênicas v-raf/genética
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas B-raf/genética
Proteínas Proto-Oncogênicas p21(ras)
Proteína Supressora de Tumor p53/genética
Proteínas Supressoras de Tumor/genética
Proteínas ras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (KRAS protein, human); 0 (Proto-Oncogene Proteins); 0 (RASSF1 protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 0 (Tumor Suppressor Proteins); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1302
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120713
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.27722


  5 / 150 MEDLINE  
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[PMID]:21403838
[Au] Autor:De Vitis S; Sonia Treglia A; Ulianich L; Turco S; Terrazzano G; Lombardi A; Miele C; Garbi C; Beguinot F; Di Jeso B
[Ad] Endereço:Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Facoltà di Scienze Matematiche Fisiche e Naturali, Università degli Studi del Salento, Lecce, Italy.
[Ti] Título:Tyr phosphatase-mediated P-ERK inhibition suppresses senescence in EIA + v-raf transformed cells, which, paradoxically, are apoptosis-protected in a MEK-dependent manner.
[So] Source:Neoplasia;13(2):120-30, 2011 Feb.
[Is] ISSN:1476-5586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activation of the Ras-Raf-extracellular signal-regulated kinase (ERK) pathway causes not only proliferation and suppression of apoptosis but also the antioncogenic response of senescence. How these contrasting effects are reconciled to achieve cell transformation and cancer formation is poorly understood. In a system of two-step carcinogenesis (dedifferentiated PC EIA, transformed PC EIA-polyoma-middle T [PC EIA + Py] and PC EIA-v-raf [PC EIA + raf] cells], v-raf cooperated with EIA by virtue of a strong prosurvival effect, not elicited by Py-middle T, evident toward serum-deprivation-and H(2)O(2)-induced apoptosis. Apoptosis was detected by DNA fragmentation and annexin V staining. The prosurvival function of v-raf was, in part, mitogen-activated protein kinase/ERK kinase (MEK)-dependent, as shown by pharmacological MEK inhibition. The MEK-dependent antiapoptotic effect of v-raf was exerted despite a lower level of P-ERK1/2 in EIA + raf cells with respect to EIA + Py/EIA cells, which was dependent on a high tyrosine phosphatase activity, as shown by orthovanadate blockade. An ERK1/2 tyrosine phosphatase was likely involved. The high tyrosine phosphatase activity was instrumental to the complete suppression of senescence, detected by ß-galactosidase activity, because tyrosine phosphatase blockade induced senescence in EIA + raf but not in EIA + Py cells. High tyrosine phosphatase activity and evasion from senescence were confirmed in an anaplastic thyroid cancer cell line. Therefore, besides EIA, EIA + raf cells suppress senescence through a new mechanism, namely, phosphatase-mediated P-ERK1/2 inhibition, but, paradoxically, retain the oncogenic effects of the Raf-ERK pathway. We propose that the survival effect of Raf is not a function of absolute P-ERK1/2 levels at a given time but is rather dynamically dependent on greater variations after an apoptotic stimulus.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/metabolismo
Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Proteínas Oncogênicas v-raf/metabolismo
Proteínas Tirosina Fosfatases/metabolismo
Neoplasias da Glândula Tireoide/enzimologia
[Mh] Termos MeSH secundário: Apoptose/genética
Linhagem Celular Tumoral
Transformação Celular Neoplásica/genética
Senescência Celular
Regulação da Expressão Gênica
Seres Humanos
Peróxido de Hidrogênio/metabolismo
Quinases de Proteína Quinase Ativadas por Mitógeno/genética
Proteínas Oncogênicas v-raf/genética
beta-Galactosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
BBX060AN9V (Hydrogen Peroxide); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.1.3.48 (Protein Tyrosine Phosphatases); EC 3.2.1.23 (beta-Galactosidase)
[Em] Mês de entrada:1106
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110316
[St] Status:MEDLINE


  6 / 150 MEDLINE  
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[PMID]:20199087
[Au] Autor:Suijkerbuijk BM; Niculescu-Duvaz I; Gaulon C; Dijkstra HP; Niculescu-Duvaz D; Ménard D; Zambon A; Nourry A; Davies L; Manne HA; Friedlos F; Ogilvie LM; Hedley D; Lopes F; Preece NP; Moreno-Farre J; Raynaud FI; Kirk R; Whittaker S; Marais R; Springer CJ
[Ad] Endereço:The Institute of Cancer Research, Cancer Research UK Centre for Cancer Therapeutics, 15 Cotswold Road, Sutton, Surrey SM2 5NG, United Kingdom.
[Ti] Título:Development of novel, highly potent inhibitors of V-RAF murine sarcoma viral oncogene homologue B1 (BRAF): increasing cellular potency through optimization of a distal heteroaromatic group.
[So] Source:J Med Chem;53(7):2741-56, 2010 Apr 08.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We describe the design, synthesis, and optimization of a series of new inhibitors of V-RAF murine sarcoma viral oncogene homologue B1 (BRAF), a kinase whose mutant form (V600E) is implicated in several types of cancer, with a particularly high frequency in melanoma. Our previously described inhibitors with a tripartite A-B-C system (where A is a hinge binding pyrido[4,5-b]imidazolone system, B is an aryl spacer group, and C is a heteroaromatic group) were potent against purified (V600E)BRAF in vitro but were less potent in accompanying cellular assays. Substitution of different aromatic heterocycles for the phenyl based C-ring is evaluated herein as a potential means of improving the cellular potencies of these inhibitors. Substituted pyrazoles, particularly 3-tert-butyl-1-aryl-1H-pyrazoles, increase the cellular potencies without detrimental effects on the potency on isolated (V600E)BRAF. Thus, compounds have been synthesized that inhibit, with low nanomolar concentrations, (V600E)BRAF, its downstream signaling in cells [as measured by the reduction of the phosphorylation of extracellular regulated kinase (ERK)], and the proliferation of mutant BRAF-dependent cells. Concomitant benefits are good oral bioavailability and high plasma concentrations in vivo.
[Mh] Termos MeSH primário: Desenho de Drogas
Proteínas Oncogênicas v-raf/química
Inibidores de Proteínas Quinases/química
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/antagonistas & inibidores
Vírus do Sarcoma Murino/enzimologia
Homologia de Sequência
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Feminino
Seres Humanos
Concentração Inibidora 50
Camundongos
Modelos Moleculares
Conformação Molecular
Inibidores de Proteínas Quinases/metabolismo
Inibidores de Proteínas Quinases/farmacocinética
Proteínas Proto-Oncogênicas B-raf/química
Proteínas Proto-Oncogênicas B-raf/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1005
[Cu] Atualização por classe:161203
[Lr] Data última revisão:
161203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100305
[St] Status:MEDLINE
[do] DOI:10.1021/jm900607f


  7 / 150 MEDLINE  
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[PMID]:18212057
[Au] Autor:Kuznetsov AV; Smigelskaite J; Doblander C; Janakiraman M; Hermann M; Wurm M; Scheidl SF; Sucher R; Deutschmann A; Troppmair J
[Ad] Endereço:Daniel Swarovski Research Laboratory, Department of General and Transplant Surgery, Innsbruck Medical University, Innrain 66, 6020 Innsbruck, Austria.
[Ti] Título:Survival signaling by C-RAF: mitochondrial reactive oxygen species and Ca2+ are critical targets.
[So] Source:Mol Cell Biol;28(7):2304-13, 2008 Apr.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Survival signaling by RAF occurs through largely unknown mechanisms. Here we provide evidence for the first time that RAF controls cell survival by maintaining permissive levels of mitochondrial reactive oxygen species (ROS) and Ca(2+). Interleukin-3 (IL-3) withdrawal from 32D cells resulted in ROS production, which was suppressed by activated C-RAF. Oncogenic C-RAF decreased the percentage of apoptotic cells following treatment with staurosporine or the oxidative stress-inducing agent tert-butyl hydroperoxide. However, it was also the case that in parental 32D cells growing in the presence of IL-3, inhibition of RAF signaling resulted in elevated mitochondrial ROS and Ca(2+) levels. Cell death is preceded by a ROS-dependent increase in mitochondrial Ca(2+), which was absent from cells expressing transforming C-RAF. Prevention of mitochondrial Ca(2+) overload after IL-3 deprivation increased cell viability. MEK was essential for the mitochondrial effects of RAF. In summary, our data show that survival control by C-RAF involves controlling ROS production, which otherwise perturbs mitochondrial Ca(2+) homeostasis.
[Mh] Termos MeSH primário: Sinalização do Cálcio/fisiologia
Mitocôndrias/metabolismo
Proteínas Oncogênicas v-raf/fisiologia
Proteínas Proto-Oncogênicas c-raf/fisiologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Proteínas Reguladoras de Apoptose/fisiologia
Sobrevivência Celular/fisiologia
Homeostase
Seres Humanos
Interleucina-3/farmacologia
Camundongos
Microscopia Confocal
Células Mieloides/citologia
Células Mieloides/efeitos dos fármacos
Células Mieloides/metabolismo
Proteínas Oncogênicas v-raf/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/fisiologia
Proteínas Proto-Oncogênicas c-raf/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-raf/genética
RNA Interferente Pequeno/farmacologia
Proteínas Recombinantes de Fusão/fisiologia
Estaurosporina/farmacologia
Superóxido Dismutase/genética
Superóxido Dismutase/fisiologia
terc-Butil Hidroperóxido/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Apoptosis Regulatory Proteins); 0 (Interleukin-3); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (Recombinant Fusion Proteins); 955VYL842B (tert-Butylhydroperoxide); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); H88EPA0A3N (Staurosporine)
[Em] Mês de entrada:0805
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080124
[St] Status:MEDLINE
[do] DOI:10.1128/MCB.00683-07


  8 / 150 MEDLINE  
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[PMID]:16945999
[Au] Autor:Letterio J; Rudikoff E; Voong N; Bauer SR
[Ad] Endereço:Case Western Reserve University, Division of Pediatric Hematology/Oncology, The Ireland Cancer Center, Cleveland, Ohio, USA.
[Ti] Título:Transforming growth factor-beta1 sensitivity is altered in Abl-Myc- and Raf-Myc-induced mouse pre-B-cell tumors.
[So] Source:Stem Cells;24(12):2611-7, 2006 Dec.
[Is] ISSN:1066-5099
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding the mechanisms leading to transformation of early B-lineage precursors is an important step leading to rational design of new treatments for precursor (pre)-B-cell leukemia. We used normal mouse pre-B cells to determine if and how transforming growth factor (TGF)-beta1 affects these precursors to the B-cell lineage and whether transformed pre-B cells respond to TGF-beta1. We found that normal pre-B cells proliferating in the presence of interleukin (IL)-7 enter cell-cycle arrest after exposure to TGF-beta1. However, clonally related IL-7-independent tumors induced by oncogenes abl + myc or raf + myc have reduced sensitivity to TGF-beta1. In contrast, tumor cells induced by myc alone remain sensitive to TGF-beta1 growth suppression. These results suggest that lesions in different molecular signaling pathways can lead to loss of TGF-beta1 sensitivity in a single cell type. The approach of using normal pre-B-cell lines and transformation by overexpression of different oncogenes provides a system to compare and contrast molecular pathways that lead to full malignancy.
[Mh] Termos MeSH primário: Linfócitos B/efeitos dos fármacos
Linfócitos B/patologia
Neoplasias/patologia
Proteína Oncogênica p55(v-myc)/genética
Proteínas Oncogênicas v-abl/genética
Proteínas Oncogênicas v-raf/genética
Fator de Crescimento Transformador beta1/farmacologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Linfócitos B/metabolismo
Proliferação Celular/efeitos dos fármacos
Transformação Celular Neoplásica
Fase G1/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Camundongos
Neoplasias/genética
Proteína Oncogênica p55(v-myc)/metabolismo
Proteínas Oncogênicas v-abl/metabolismo
Proteínas Oncogênicas v-raf/metabolismo
Receptores de Interleucina-7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Oncogene Protein p55(v-myc)); 0 (Oncogene Proteins v-abl); 0 (Receptors, Interleukin-7); 0 (Transforming Growth Factor beta1); EC 2.7.11.1 (Oncogene Proteins v-raf)
[Em] Mês de entrada:0702
[Cu] Atualização por classe:150813
[Lr] Data última revisão:
150813
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060902
[St] Status:MEDLINE


  9 / 150 MEDLINE  
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[PMID]:16491116
[Au] Autor:Hartl M; Karagiannidis AI; Bister K
[Ad] Endereço:Institute of Biochemistry and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria. markus.hartl@uibk.ac.at
[Ti] Título:Cooperative cell transformation by Myc/Mil(Raf) involves induction of AP-1 and activation of genes implicated in cell motility and metastasis.
[So] Source:Oncogene;25(29):4043-55, 2006 Jul 06.
[Is] ISSN:0950-9232
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Avian fibroblasts transformed simultaneously by the v-myc and v-mil(raf) oncogenes of acute leukemia and carcinoma virus MH2 contain elevated levels of c-Fos and c-Jun, major components of the transcription factor complex AP-1. To define specific transcriptional targets in these cells, subtractive hybridization techniques were employed leading to the identification of strongly upregulated genes including OPN (osteopontin), 126MRP, and rac2. OPN is a cytokine and cell attachment protein which has been implicated in human tumor progression and metastasis, the calcium binding 126MRP protein is related to the human S100 protein family involved in invasive cell growth, and the Rac2 protein belongs to the Rho family of small GTPases regulating actin reorganization and cell migration. Promoter analysis indicated that OPN activation is mediated by a non-consensus AP-1 binding site located close to the transcription start site. Electrophoretic mobility shift assays, chromatin immunoprecipitation and transcriptional reporter gene analyses showed that c-Fos and c-Jun bind specifically to this site and that c-Fos efficiently transactivates the OPN promoter. High-level expression of OPN, 126MRP, or Rac2 proteins from a retroviral vector led to partial cell transformation, documented by morphological changes and anchorage-independent growth. The specific activation in v-myc/v-mil(raf)-transformed cells of target genes with intrinsic oncogenic potential may provide an explanation for the longstanding observation that concomitant expression of these oncogenes leads to strongly enhanced oncogenicity in vivo and in vitro compared to cell transformation by v-myc or v-mil(raf) alone.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica
Transformação Celular Viral
Fibroblastos/metabolismo
Regulação Neoplásica da Expressão Gênica
Genes myc
Metástase Neoplásica
Proteínas Oncogênicas v-raf/metabolismo
Fator de Transcrição AP-1/metabolismo
[Mh] Termos MeSH secundário: Alpharetrovirus/genética
Alpharetrovirus/metabolismo
Animais
Movimento Celular/genética
Transformação Celular Neoplásica/genética
Transformação Celular Viral/genética
Células Cultivadas
Embrião de Galinha
Galinhas
Coturnix
Fibroblastos/patologia
Genes jun/genética
Genes myc/genética
Seres Humanos
Metástase Neoplásica/genética
Proteínas Oncogênicas v-raf/genética
Osteopontina
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-fos/genética
Proteínas Proto-Oncogênicas c-fos/metabolismo
Sialoglicoproteínas/biossíntese
Sialoglicoproteínas/genética
Fator de Transcrição AP-1/genética
Regulação para Cima
Proteínas rac de Ligação ao GTP/genética
Proteínas rac de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-fos); 0 (SPP1 protein, human); 0 (Sialoglycoproteins); 0 (Transcription Factor AP-1); 106441-73-0 (Osteopontin); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 3.6.1.- (rac2 GTP-binding protein); EC 3.6.5.2 (rac GTP-Binding Proteins)
[Em] Mês de entrada:0608
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060224
[St] Status:MEDLINE


  10 / 150 MEDLINE  
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[PMID]:16273242
[Au] Autor:Ogawa K; Sun C; Horii A
[Ad] Endereço:Department of Molecular Pathology, Tohoku University School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.
[Ti] Título:Exploration of genetic alterations in human endometrial cancer and melanoma: distinct tumorigenic pathways that share a frequent abnormal PI3K/AKT cascade.
[So] Source:Oncol Rep;14(6):1481-5, 2005 Dec.
[Is] ISSN:1021-335X
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Mutations of RAS, RAF, and PTEN, all important members of the RAS/MAPK and PI3K/AKT cascades, are reported in a variety of human tumors, including melanomas and endometrial cancer. In endometrial cancer, mutually exclusive mutations of PTEN and KRAS have been reported. On the other hand, mutation of BRAF is highly frequent, and mutually exclusive mutations of BRAF and NRAS have also been reported in melanomas. In this study, we elucidated the involvement of the up-regulation of RAS/MAPK and PI3K/AKT cascades in the pathogenesis of endometrial cancer and melanoma by analyzing the genes and molecules in these cascades. Twelve cell lines, six melanoma and six endometrial cancer, were analyzed; 4 (67%) of the 6 melanomas had gene mutations in the RAS/MAPK cascade, and a decrease or loss of PTEN expression was also observed. These results suggested that simultaneous up-regulations in these two cascades play important roles in carcinogenesis of melanocytes. However, no activation of AKT by phosphorylation was observed. On the other hand, 4 (67%) of the 6 endometrial cancer cell lines had mutually exclusive up-regulations in these cascades. However, two cell lines with up-regulation of the PI3K/AKT cascade also had up-regulation in the RAS/MAPK cascade induced by inactivation of DUSP6. These results suggest that simultaneous up-regulation of RAS/MAPK and PI3K/AKT cascades are crucial events in the pathogenesis of melanocytes, whereas up-regulation of either the RAS/MAPK or PI3K/AKT cascade is crucial for the majority of endometrial cancers.
[Mh] Termos MeSH primário: Neoplasias do Endométrio/genética
Melanoma/genética
Mutação
[Mh] Termos MeSH secundário: Sequência de Bases
Western Blotting
Linhagem Celular Tumoral
Análise Mutacional de DNA
Neoplasias do Endométrio/metabolismo
Neoplasias do Endométrio/patologia
Feminino
Seres Humanos
Melanoma/metabolismo
Melanoma/patologia
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Proteína Oncogênica v-akt/metabolismo
Proteínas Oncogênicas v-raf/genética
PTEN Fosfo-Hidrolase/genética
PTEN Fosfo-Hidrolase/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas A-raf/genética
Proteínas Proto-Oncogênicas B-raf/genética
Transdução de Sinais
Proteínas ras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Oncogene Protein v-akt); EC 2.7.11.1 (Oncogene Proteins v-raf); EC 2.7.11.1 (Proto-Oncogene Proteins A-raf); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:0601
[Cu] Atualização por classe:120621
[Lr] Data última revisão:
120621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051108
[St] Status:MEDLINE



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