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Pesquisa : D12.776.260.103.500.625 [Categoria DeCS]
Referências encontradas : 724 [refinar]
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[PMID]:27773673
[Au] Autor:Xiao D; Yue M; Su H; Ren P; Jiang J; Li F; Hu Y; Du H; Liu H; Qing G
[Ad] Endereço:Zhongnan Hospital of Wuhan University, Wuhan 430071, China; Medical Research Institute, Wuhan University, Wuhan 430071, China.
[Ti] Título:Polo-like Kinase-1 Regulates Myc Stabilization and Activates a Feedforward Circuit Promoting Tumor Cell Survival.
[So] Source:Mol Cell;64(3):493-506, 2016 Nov 03.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MYCN amplification in human cancers predicts poor prognosis and resistance to therapy. However, pharmacological strategies that directly target N-Myc, the protein encoded by MYCN, remain elusive. Here, we identify a molecular mechanism responsible for reciprocal activation between Polo-like kinase-1 (PLK1) and N-Myc. PLK1 specifically binds to the SCF ubiquitin ligase, phosphorylates it, and promotes its autopolyubiquitination and proteasomal degradation, counteracting Fbw7-mediated degradation of N-Myc and additional substrates, including cyclin E and Mcl1. Stabilized N-Myc in turn directly activates PLK1 transcription, constituting a positive feedforward regulatory loop that reinforces Myc-regulated oncogenic programs. Inhibitors of PLK1 preferentially induce potent apoptosis of MYCN-amplified tumor cells from neuroblastoma and small cell lung cancer and synergistically potentiate the therapeutic efficacies of Bcl2 antagonists. These findings reveal a PLK1-Fbw7-Myc signaling circuit that underlies tumorigenesis and validate PLK1 inhibitors, alone or with Bcl2 antagonists, as potential effective therapeutics for MYC-overexpressing cancers.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Proteínas de Ciclo Celular/genética
Proteínas F-Box/genética
Retroalimentação Fisiológica
Regulação Neoplásica da Expressão Gênica
Proteína Proto-Oncogênica N-Myc/genética
Neuroblastoma/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/patologia
Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Proteínas de Ciclo Celular/antagonistas & inibidores
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Sinergismo Farmacológico
Proteínas F-Box/metabolismo
Proteína 7 com Repetições F-Box-WD
Seres Humanos
Camundongos Nus
Proteína Proto-Oncogênica N-Myc/antagonistas & inibidores
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/mortalidade
Neuroblastoma/patologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurônios/patologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Pteridinas/farmacologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Sulfonamidas/farmacologia
Análise de Sobrevida
Transcrição Genética
Carga Tumoral/efeitos dos fármacos
Ubiquitina-Proteína Ligases/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BCL2 protein, human); 0 (BI 6727); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Cell Cycle Proteins); 0 (F-Box Proteins); 0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (MYCN protein, human); 0 (N-Myc Proto-Oncogene Protein); 0 (Proto-Oncogene Proteins); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Pteridines); 0 (RNA, Small Interfering); 0 (Sulfonamides); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1); N54AIC43PW (venetoclax)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180114
[Lr] Data última revisão:
180114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


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[PMID]:29277758
[Au] Autor:Ahn EH; Lee MB; Seo DJ; Lee J; Kim Y; Gupta K
[Ad] Endereço:Department of Pathology, School of Medicine, University of Washington, Seattle, WA, U.S.A. ahneun@uw.edu.
[Ti] Título:Sphingosine Induces Apoptosis and Down-regulation of in PAX3-FOXO1-positive Alveolar Rhabdomyosarcoma Cells Irrespective of Mutation.
[So] Source:Anticancer Res;38(1):71-76, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Rhabdomyosarcoma is the most common type of pediatric soft-tissue sarcoma. Among the subsets of this disease, alveolar rhabdomyosarcoma (ARMS) expressing paired box 3 (PAX3) and forkhead box O1 (PAX3-FOXO1) fusion oncoprotein has the worst prognosis. The goal of this study was to investigate the chemotherapeutic effects of sphingosine on PAX3-FOXO1-positive ARMS cells [tumor protein p53 (TP53)-mutated RH30 and TP53 wild-type RH18 cells]. MATERIALS AND METHODS: The proliferation, cell death, apoptosis, cell cycle, and MYCN proto-oncogene (MYCN) expression of RH30 and RH18 cells were determined. RESULTS: Sphingosine inhibited the growth and caused cell death in a dose-dependent manner in both cell lines. Sphingosine triggered cell death by inducing apoptosis without affecting the cell cycle. MYCN expression was down-regulated within 2 and 4 h of sphingosine treatment in both RH30 and RH18 cells. CONCLUSION: Sphingosine exerts antiproliferative and pro-apoptotic effects via MYCN down-regulation independently of TP53 mutation status in PAX3-FOXO1-positive ARMS cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Proteína Proto-Oncogênica N-Myc/genética
Rabdomiossarcoma Alveolar/genética
Esfingosina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Proteína Forkhead Box O1/metabolismo
Seres Humanos
Mutação
Fator de Transcrição PAX3/metabolismo
Rabdomiossarcoma Alveolar/metabolismo
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (FOXO1 protein, human); 0 (Forkhead Box Protein O1); 0 (MYCN protein, human); 0 (N-Myc Proto-Oncogene Protein); 0 (PAX3 Transcription Factor); 0 (PAX3 protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29061788
[Au] Autor:Pohl A; Kappler R; Mühling J; VON Schweinitz D; Berger M
[Ad] Endereço:Department of Pediatric Surgery, Dr von Hauner Children's Hospital, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
[Ti] Título:Expression of Truncated Neurokinin-1 Receptor in Childhood Neuroblastoma is Independent of Tumor Biology and Stage.
[So] Source:Anticancer Res;37(11):6079-6085, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Neuroblastoma is an embryonal malignancy arising from the aberrant growth of neural crest progenitor cells of the sympathetic nervous system. The tachykinin receptor 1 (TACR1) - substance P complex is associated with tumoral angiogenesis and cell proliferation in a variety of cancer types. Inhibition of TACR1 was recently described to impede growth of NB cell lines. However, the relevance of TACR1 in clinical settings is unknown. PATIENTS AND METHODS: We investigated gene expression levels of full-length and truncated TACR1 in 59 neuroblastomas and correlated these data with the patients' clinical parameters such as outcome, metastasis, International Neuroblastoma Staging System (INSS) status, MYCN proto-oncogene, bHLH transcription factor (MYCN) status, gender and age. RESULTS: Our results indicated that TACR1 is ubiquitously expressed in neuroblastoma but expression levels are independent of clinical parameters. CONCLUSION: Our data suggest that TACR1 might serve as a potent anticancer target in a large variety of patients with neuroblastoma, independent of tumor biology and clinical stage.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Regulação Neoplásica da Expressão Gênica
Neuroblastoma/metabolismo
Receptores da Neurocinina-1/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Biomarcadores Tumorais/genética
Criança
Pré-Escolar
Feminino
Seguimentos
Seres Humanos
Lactente
Recém-Nascido
Metástase Linfática
Masculino
Proteína Proto-Oncogênica N-Myc/genética
Proteína Proto-Oncogênica N-Myc/metabolismo
Estadiamento de Neoplasias
Neuroblastoma/patologia
Prognóstico
Receptores da Neurocinina-1/genética
Taxa de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MYCN protein, human); 0 (N-Myc Proto-Oncogene Protein); 0 (Receptors, Neurokinin-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:28927789
[Au] Autor:Takahashi N; Koyama S; Hasegawa S; Yamasaki M; Imai M
[Ad] Endereço:Laboratory of Physiological Chemistry, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa, Tokyo 142-8501, Japan. Electronic address: t-noriko@hoshi.ac.jp.
[Ti] Título:Anticancer efficacy of p-dodecylaminophenol against high-risk and refractory neuroblastoma cells in vitro and in vivo.
[So] Source:Bioorg Med Chem Lett;27(20):4664-4672, 2017 10 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma is an aggressive and drug-resistant refractory cancer. The human high-risk neuroblastoma cell line, SK-N-AS (non-amplified N-myc) is derived from stromal cells and it is resistant to treatment with retinoic acid (1, RA), which is a chemotherapeutic agent used to induce neuronal cellular differentiation of neuroblastomas. We have developed p-dodecylaminophenol (3, p-DDAP), based on N-(4-hydroxyphenyl)retinamide (2, 4-HPR), a synthetic amide of 1, since 1 and 2 are associated with the side-effect of nyctalopia. In order to evaluate the effects of 3 on high-risk neuroblastomas, we employed SK-N-AS cells as well asa second high-risk human neuroblastoma cell line, IMR-32, which is derived from neuronal cells (amplified N-myc, drug sensitive). Compound 3 suppressed cell growth of SK-N-AS and IMR-32 cells more effectively than 1, 2, p-decylaminophenol (4, p-DAP), N-(4-hydroxyphenyl)dodecananamide (5, 4-HPDD) or N-(4-hydroxyphenyl)decananamide (6, 4-HPD). In SK-N-AS cells, 3 induced G /G arrest and apoptosis to a greater extent than 1 and 2. In IMR-32 cells, 3 induced apoptosis to a similar extent as 1 and 2, potentially by inhibiting N-myc expression. In addition, i.p. administration of 3 suppressed tumor growth in SK-N-AS-implanted mice in vivo. Since 3 showed no effects on blood retinol concentrations, in contrast to reductions following the administration of 2, it exhibited excellent anticancer efficacy against high-risk neuroblastoma SK-N-AS and IMR-32 expressing distinct levels of N-myc. Compound 3 may have potential for clinical use in the treatment of refractory neuroblastoma with reduced side effects.
[Mh] Termos MeSH primário: Aminofenóis/química
Aminofenóis/farmacologia
Antineoplásicos/química
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
[Mh] Termos MeSH secundário: Aminofenóis/uso terapêutico
Animais
Antineoplásicos/uso terapêutico
Caspase 3/metabolismo
Linhagem Celular Tumoral
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Proteína Proto-Oncogênica N-Myc/genética
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/metabolismo
Neuroblastoma/patologia
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-dodecylaminophenol); 0 (Aminophenols); 0 (Antineoplastic Agents); 0 (N-Myc Proto-Oncogene Protein); 0 (Proto-Oncogene Proteins c-bcl-2); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


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[PMID]:28898695
[Au] Autor:Bosse KR; Raman P; Zhu Z; Lane M; Martinez D; Heitzeneder S; Rathi KS; Kendsersky NM; Randall M; Donovan L; Morrissy S; Sussman RT; Zhelev DV; Feng Y; Wang Y; Hwang J; Lopez G; Harenza JL; Wei JS; Pawel B; Bhatti T; Santi M; Ganguly A; Khan J; Marra MA; Taylor MD; Dimitrov DS; Mackall CL; Maris JM
[Ad] Endereço:Division of Oncology and Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Colket Translational Research Building, 3501 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia,
[Ti] Título:Identification of GPC2 as an Oncoprotein and Candidate Immunotherapeutic Target in High-Risk Neuroblastoma.
[So] Source:Cancer Cell;32(3):295-309.e12, 2017 Sep 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We developed an RNA-sequencing-based pipeline to discover differentially expressed cell-surface molecules in neuroblastoma that meet criteria for optimal immunotherapeutic target safety and efficacy. Here, we show that GPC2 is a strong candidate immunotherapeutic target in this childhood cancer. We demonstrate high GPC2 expression in neuroblastoma due to MYCN transcriptional activation and/or somatic gain of the GPC2 locus. We confirm GPC2 to be highly expressed on most neuroblastomas, but not detectable at appreciable levels in normal childhood tissues. In addition, we demonstrate that GPC2 is required for neuroblastoma proliferation. Finally, we develop a GPC2-directed antibody-drug conjugate that is potently cytotoxic to GPC2-expressing neuroblastoma cells. Collectively, these findings validate GPC2 as a non-mutated neuroblastoma oncoprotein and candidate immunotherapeutic target.
[Mh] Termos MeSH primário: Glipicanas/metabolismo
Imunoterapia
Terapia de Alvo Molecular
Neuroblastoma/imunologia
Neuroblastoma/terapia
Proteínas Oncogênicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Antineoplásicos/metabolismo
Morte Celular
Linhagem Celular Tumoral
Membrana Celular/metabolismo
Proliferação Celular
Criança
Regulação Neoplásica da Expressão Gênica
Genoma Humano
Seres Humanos
Camundongos Endogâmicos NOD
Camundongos SCID
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/genética
Neuroblastoma/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neoplasm); 0 (GPC2 protein, human); 0 (Glypicans); 0 (MYCN protein, human); 0 (N-Myc Proto-Oncogene Protein); 0 (Oncogene Proteins); 0 (RNA, Messenger)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE


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[PMID]:28867147
[Au] Autor:Zhu S; Zhang X; Weichert-Leahey N; Dong Z; Zhang C; Lopez G; Tao T; He S; Wood AC; Oldridge D; Ung CY; van Ree JH; Khan A; Salazar BM; Lummertz da Rocha E; Zimmerman MW; Guo F; Cao H; Hou X; Weroha SJ; Perez-Atayde AR; Neuberg DS; Meves A; McNiven MA; van Deursen JM; Li H; Maris JM; Look AT
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Mayo Clinic Cancer Center, Rochester, MN 55902, USA. Electronic address: zhu.shizhen@mayo.edu.
[Ti] Título:LMO1 Synergizes with MYCN to Promote Neuroblastoma Initiation and Metastasis.
[So] Source:Cancer Cell;32(3):310-323.e5, 2017 Sep 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A genome-wide association study identified LMO1, which encodes an LIM-domain-only transcriptional cofactor, as a neuroblastoma susceptibility gene that functions as an oncogene in high-risk neuroblastoma. Here we show that dßh promoter-mediated expression of LMO1 in zebrafish synergizes with MYCN to increase the proliferation of hyperplastic sympathoadrenal precursor cells, leading to a reduced latency and increased penetrance of neuroblastomagenesis. The transgenic expression of LMO1 also promoted hematogenous dissemination and distant metastasis, which was linked to neuroblastoma cell invasion and migration, and elevated expression levels of genes affecting tumor cell-extracellular matrix interaction, including loxl3, itga2b, itga3, and itga5. Our results provide in vivo validation of LMO1 as an important oncogene that promotes neuroblastoma initiation, progression, and widespread metastatic dissemination.
[Mh] Termos MeSH primário: Carcinogênese/patologia
Proteínas de Ligação a DNA/metabolismo
Proteínas com Domínio LIM/metabolismo
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/metabolismo
Neuroblastoma/patologia
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Carcinogênese/metabolismo
Linhagem Celular Tumoral
Movimento Celular/genética
Matriz Extracelular/metabolismo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Hiperplasia
Modelos Biológicos
Invasividade Neoplásica
Metástase Neoplásica
Neuroblastoma/genética
Transdução de Sinais/genética
Transgenes
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (LIM Domain Proteins); 0 (LMO1 protein, human); 0 (MYCN protein, human); 0 (N-Myc Proto-Oncogene Protein); 0 (Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


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[PMID]:28817597
[Au] Autor:Pipelers P; Clement L; Vynck M; Hellemans J; Vandesompele J; Thas O
[Ad] Endereço:Department of Mathematical Modelling, Statistics and Bioinformatics, Ghent University, Ghent, Belgium.
[Ti] Título:A unified censored normal regression model for qPCR differential gene expression analysis.
[So] Source:PLoS One;12(8):e0182832, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reverse transcription quantitative polymerase chain reaction (RT-qPCR) is considered as the gold standard for accurate, sensitive, and fast measurement of gene expression. Prior to downstream statistical analysis, RT-qPCR fluorescence amplification curves are summarized into one single value, the quantification cycle (Cq). When RT-qPCR does not reach the limit of detection, the Cq is labeled as "undetermined". Current state of the art qPCR data analysis pipelines acknowledge the importance of normalization for removing non-biological sample to sample variation in the Cq values. However, their strategies for handling undetermined Cq values are very ad hoc. We show that popular methods for handling undetermined values can have a severe impact on the downstream differential expression analysis. They introduce a considerable bias and suffer from a lower precision. We propose a novel method that unites preprocessing and differential expression analysis in a single statistical model that provides a rigorous way for handling undetermined Cq values. We compare our method with existing approaches in a simulation study and on published microRNA and mRNA gene expression datasets. We show that our method outperforms traditional RT-qPCR differential expression analysis pipelines in the presence of undetermined values, both in terms of accuracy and precision.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica/métodos
Técnicas de Diagnóstico Molecular/métodos
Neuroblastoma/genética
Reação em Cadeia da Polimerase/métodos
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Biomarcadores Tumorais/metabolismo
Criança
Pré-Escolar
Perfilação da Expressão Gênica/normas
Seres Humanos
MicroRNAs/genética
Técnicas de Diagnóstico Molecular/normas
Proteína Proto-Oncogênica N-Myc/genética
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/diagnóstico
Neuroblastoma/metabolismo
Reação em Cadeia da Polimerase/normas
Padrões de Referência
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MYCN protein, human); 0 (MicroRNAs); 0 (N-Myc Proto-Oncogene Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182832


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[PMID]:28807939
[Au] Autor:Tsubota S; Kishida S; Shimamura T; Ohira M; Yamashita S; Cao D; Kiyonari S; Ushijima T; Kadomatsu K
[Ad] Endereço:Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
[Ti] Título:PRC2-Mediated Transcriptomic Alterations at the Embryonic Stage Govern Tumorigenesis and Clinical Outcome in MYCN-Driven Neuroblastoma.
[So] Source:Cancer Res;77(19):5259-5271, 2017 Oct 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pediatric cancers such as neuroblastoma are thought to involve a dysregulation of embryonic development. However, it has been difficult to identify the critical events that trigger tumorigenesis and differentiate them from normal development. In this study, we report the establishment of a spheroid culture method that enriches early-stage tumor cells from TH-MYCN mice, a preclinical model of neuroblastoma. Using this method, we found that tumorigenic cells were evident as early as day E13.5 during embryo development, when the MYC and PRC2 transcriptomes were significantly altered. Ezh2, an essential component of PRC2, was expressed in embryonic and postnatal tumor lesions and physically associated with N-MYC and we observed that H3K27me3 was increased at PRC2 target genes. PRC2 inhibition suppressed sphere formation, derepressed its target genes, and suppressed tumor growth. In clinical specimens, expression of MYC and PRC2 target genes correlated strongly and predicted survival outcomes. Together, our findings highlighted PRC2-mediated transcriptional control during embryogenesis as a critical step in the development and clinical outcome of neuroblastoma. .
[Mh] Termos MeSH primário: Carcinogênese/patologia
Embrião de Mamíferos/patologia
Regulação Neoplásica da Expressão Gênica
Proteína Proto-Oncogênica N-Myc/genética
Neuroblastoma/patologia
Complexo Repressor Polycomb 2/metabolismo
Transcriptoma
[Mh] Termos MeSH secundário: Animais
Biomarcadores Tumorais/genética
Carcinogênese/metabolismo
Embrião de Mamíferos/metabolismo
Feminino
Seres Humanos
Masculino
Camundongos
Estadiamento de Neoplasias
Neuroblastoma/genética
Neuroblastoma/metabolismo
Complexo Repressor Polycomb 2/genética
Prognóstico
Taxa de Sobrevida
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (N-Myc Proto-Oncogene Protein); EC 2.1.1.43 (Polycomb Repressive Complex 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-3144


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[PMID]:28796037
[Au] Autor:Ruan L; Yang Y; Huang Y; Ding L; Zhang C; Wu X
[Ad] Endereço:Department of Gerontology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Functional prediction of miR-3144-5p in human cardiac myocytes based on transcriptome sequencing and bioinformatics.
[So] Source:Medicine (Baltimore);96(32):e7539, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: RAN guanine nucleotide release factor (RANGRF) encoding protein MOG1 plays an important role in cardiac arrhythmia, so we intended to investigate the regulatory miRNA of RANGRF and explore its potential regulatory mechanism in arrhythmogenesis. METHODS: Based on bioinformatic analysis, miR-3144-5p was predicted to be a regulatory miRNA of RANGRF, which were then validated through a dual-luciferase reporter plasmid assay. Subsequently, the expression level of miR-3144-5p in human cardiac myocytes (HCMs) was detected, followed by cell transfection with miR-3144-5p mimics. Transcriptome sequencing was then performed in HCMs with or without transfection. The sequencing results were subjected to bioinformatic analyses, including differentially expressed gene (DEG) analysis, functional enrichment analysis, protein-protein interaction (PPI) network analysis, miRNA-target gene analysis, and miRNA-transcription factor (TF)-target gene coregulatory network analysis. RESULTS: There really existed a regulatory relation between miR-3144-5p and RANGRF. The expression level of miR-3144-5p was low in HCMs. After cell transfection, miR-3144-5p expression level significantly increased in HCMs. Bioinformatic analyses of the transcriptome sequencing results identified 300 upregulated and 271 downregulated DEGs between miR-3144-5p mimic and control group. The upregulated genes ISL1 and neuregulin 1 (NRG1) were significantly enriched in cardiac muscle cell myoblast differentiation (GO:0060379). CCL21 was one of the hub genes in the PPI network and also a target gene of miR-3144-5p. Moreover, the TF of v-Myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog (MYCN) was involved in the miR-3144-5p-TF-target gene coregulatory network and interacted with the target genes of miR-3144-5p. CONCLUSION: ISL1, NRG1, CCL21, and MYCN were differentially expressed in the miR-3144-5p mimic group, suggesting that miR-3144-5p overexpression plays a role in HCMs by regulating these genes and TF. This study may provide new insight into the mechanisms behind the progression of cardiac arrhythmia.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
MicroRNAs/biossíntese
Miócitos Cardíacos/metabolismo
Proteína ran de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Quimiocina CCL21/biossíntese
Perfilação da Expressão Gênica
Seres Humanos
Proteínas com Homeodomínio LIM/biossíntese
Proteína Proto-Oncogênica N-Myc/biossíntese
Neuregulina-1/biossíntese
Fatores de Transcrição/biossíntese
Transcriptoma
Regulação para Cima
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL21 protein, human); 0 (Chemokine CCL21); 0 (LIM-Homeodomain Proteins); 0 (MYCN protein, human); 0 (MicroRNAs); 0 (N-Myc Proto-Oncogene Protein); 0 (NRG1 protein, human); 0 (Neuregulin-1); 0 (Transcription Factors); 0 (insulin gene enhancer binding protein Isl-1); EC 3.6.1.- (RANGNRF protein, human); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007539


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[PMID]:28787429
[Au] Autor:Almeida GS; Panek R; Hallsworth A; Webber H; Papaevangelou E; Boult JK; Jamin Y; Chesler L; Robinson SP
[Ad] Endereço:Division of Radiotherapy &Imaging, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.
[Ti] Título:Pre-clinical imaging of transgenic mouse models of neuroblastoma using a dedicated 3-element solenoid coil on a clinical 3T platform.
[So] Source:Br J Cancer;117(6):791-800, 2017 Sep 05.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The use of clinical MRI scanners to conduct pre-clinical research facilitates comparisons with clinical studies. Here the utility and sensitivity of anatomical and functional MRI data/biomarkers acquired from transgenic mouse models of neuroblastoma using a dedicated radiofrequency (RF) coil on a clinical 3T scanner was evaluated. METHODS: Multiparametric MRI of transgenic mice bearing abdominal neuroblastomas was performed at 3T, and data cross-referenced to that acquired from the same mice on a pre-clinical 7T MRI system. T -weighted imaging, quantitation of the native longitudinal relaxation time (T ) and the transverse relaxation rate (R *), and dynamic contrast-enhanced (DCE)-MRI, was used to assess tumour volume, phenotype and response to cyclophosphamide or cabozantinib. RESULTS: Excellent T -weighted image contrast enabled clear tumour delineation at 3T. Significant correlations of tumour volume (R=0.98, P<0.0001) and R * (R=0.87, P<0.002) measured at 3 and 7T were established. Mice with neuroblastomas harbouring the anaplastic lymphoma kinase mutation exhibited a significantly slower R * (P<0.001), consistent with impaired tumour perfusion. DCE-MRI was performed simultaneously on three transgenic mice, yielding estimates of K for each tumour (median K values of 0.202, 0.168 and 0.114 min ). Cyclophosphamide elicited a significant reduction in both tumour burden (P<0.002) and native T (P<0.01), whereas cabozantinib induced significant (P<0.01) tumour growth delay. CONCLUSIONS: Simultaneous multiparametric MRI of multiple tumour-bearing animals using this coil arrangement at 3T can provide high efficiency/throughput for both phenotypic characterisation and evaluation of novel therapeutics, and facilitate the introduction of functional MRI biomarkers into aligned imaging-embedded clinical trials.
[Mh] Termos MeSH primário: Imagem por Ressonância Magnética/métodos
Imãs
Neuroblastoma/diagnóstico por imagem
Neoplasias Gástricas/diagnóstico por imagem
[Mh] Termos MeSH secundário: Anilidas/uso terapêutico
Animais
Antineoplásicos/uso terapêutico
Meios de Contraste
Ciclofosfamida/uso terapêutico
Modelos Animais de Doenças
Feminino
Imagem por Ressonância Magnética/instrumentação
Masculino
Camundongos
Camundongos Transgênicos
Mutação
Proteína Proto-Oncogênica N-Myc/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/genética
Neuroblastoma/patologia
Imagens de Fantasmas
Fenótipo
Piridinas/uso terapêutico
Receptores Proteína Tirosina Quinases/genética
Razão Sinal-Ruído
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
Neoplasias Gástricas/patologia
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Antineoplastic Agents); 0 (Contrast Media); 0 (MYCN protein, mouse); 0 (N-Myc Proto-Oncogene Protein); 0 (Pyridines); 1C39JW444G (cabozantinib); 8N3DW7272P (Cyclophosphamide); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (anaplastic lymphoma kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.251



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