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[PMID]:29384978
[Au] Autor:Nishiwaki S; Sugiura I; Miyata Y; Saito S; Sawa M; Nishida T; Miyamura K; Kuwatsuka Y; Kohno A; Yuge M; Kasai M; Iida H; Kurahashi S; Osaki M; Goto T; Terakura S; Murata M; Nishikawa H; Kiyoi H
[Ad] Endereço:Center for Advanced Medicine and Clinical Research, Nagoya University Hospital, Nagoya.
[Ti] Título:Efficacy and safety of autologous peripheral blood stem cell transplantation for Philadelphia chromosome-positive acute lymphoblastic leukemia: A study protocol for a multicenter exploratory prospective study (Auto-Ph17 study).
[So] Source:Medicine (Baltimore);96(52):e9568, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The prognosis of Philadelphia chromosome positive acute lymphoblastic leukemia (Ph + ALL) has been dramatically improved since the introduction of tyrosine kinase inhibitors (TKIs). Although allogeneic hematopoietic cell transplantation (allo-HCT) is a major treatment option, the role of autologous peripheral blood stem cell transplantation (auto-PBSCT) has been reconsidered, especially in patients who achieved early molecular remission. METHODS AND ANALYSIS: This is a multicenter exploratory study for Ph + ALL patients aged between 55 and 70 years who achieved complete molecular remission within 3 cycles of chemotherapy. The target sample size is 5, and the registration period is 2 years. The primary endpoint is Day100- mortality after transplantation, and the secondary endpoints are survival, relapse rate, nonrelapse mortality, and adverse events.This study is divided into 3 phases: peripheral blood stem cell harvest, transplantation, and maintenance. Chemomobilization is performed using a combination of cyclophosphamide (CPM), doxorubicin, vincristine (VCR), and prednisolone (PSL). As a preparative regimen, the LEED regimen is used, which consists of melphalan, CPM, etoposide, and dexamethasone. Twelve cycles of maintenance therapy using a combination of VCR, PSL, and dasatinib are performed.In association with relapse, the minimal residual disease (MRD) of BCR-ABL chimeric gene and T-cell subsets are analyzed both before and after auto-PBSCT. ETHICS AND DISSEMINATION: The protocol was approved by the institutional review board of Nagoya University Hospital and all the participating hospitals. Written informed consent was obtained from all patients before registration, in accordance with the Declaration of Helsinki. Results of the study will be disseminated via publications in peer-reviewed journals. TRIAL REGISTRATION: Trial registration number UMIN000026445.
[Mh] Termos MeSH primário: Transplante de Células-Tronco de Sangue Periférico/mortalidade
Transplante de Células-Tronco de Sangue Periférico/métodos
Cromossomo Filadélfia
Leucemia-Linfoma Linfoblástico de Células Precursoras/mortalidade
Leucemia-Linfoma Linfoblástico de Células Precursoras/terapia
[Mh] Termos MeSH secundário: Idoso
Progressão da Doença
Feminino
Genes abl/fisiologia
Seres Humanos
Imunossupressores/administração & dosagem
Masculino
Meia-Idade
Transplante de Células-Tronco de Sangue Periférico/efeitos adversos
Estudos Prospectivos
Proteínas Proto-Oncogênicas c-bcr/biossíntese
Projetos de Pesquisa
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Immunosuppressive Agents); EC 2.7.11.1 (BCR protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-bcr)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009568


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[PMID]:28628091
[Au] Autor:Dolezal E; Infantino S; Drepper F; Börsig T; Singh A; Wossning T; Fiala GJ; Minguet S; Warscheid B; Tarlinton DM; Jumaa H; Medgyesi D; Reth M
[Ad] Endereço:Department for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
[Ti] Título:The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex.
[So] Source:Nat Immunol;18(8):911-920, 2017 Aug.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Developing pre-B cells in the bone marrow alternate between proliferation and differentiation phases. We found that protein arginine methyl transferase 1 (PRMT1) and B cell translocation gene 2 (BTG2) are critical components of the pre-B cell differentiation program. The BTG2-PRMT1 module induced a cell-cycle arrest of pre-B cells that was accompanied by re-expression of Rag1 and Rag2 and the onset of immunoglobulin light chain gene rearrangements. We found that PRMT1 methylated cyclin-dependent kinase 4 (CDK4), thereby preventing the formation of a CDK4-Cyclin-D3 complex and cell cycle progression. Moreover, BTG2 in concert with PRMT1 efficiently blocked the proliferation of BCR-ABL1-transformed pre-B cells in vitro and in vivo. Our results identify a key molecular mechanism by which the BTG2-PRMT1 module regulates pre-B cell differentiation and inhibits pre-B cell leukemogenesis.
[Mh] Termos MeSH primário: Proliferação Celular/genética
Ciclina D3/metabolismo
Quinase 4 Dependente de Ciclina/metabolismo
Proteínas Imediatamente Precoces/genética
Linfopoese/genética
Células Precursoras de Linfócitos B/metabolismo
Proteína-Arginina N-Metiltransferases/genética
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Animais
Pontos de Checagem do Ciclo Celular
Diferenciação Celular/genética
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Citometria de Fluxo
Técnicas de Silenciamento de Genes
Rearranjo Gênico do Linfócito B/genética
Genes abl/genética
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Proteínas Imediatamente Precoces/metabolismo
Cadeias Leves de Imunoglobulina/genética
Espectrometria de Massas
Camundongos
Células Precursoras de Linfócitos B/citologia
Proteína-Arginina N-Metiltransferases/metabolismo
RNA Interferente Pequeno
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Btg2 protein, mouse); 0 (Ccnd3 protein, mouse); 0 (Cyclin D3); 0 (DNA-Binding Proteins); 0 (Homeodomain Proteins); 0 (Immediate-Early Proteins); 0 (Immunoglobulin Light Chains); 0 (RNA, Small Interfering); 0 (Rag2 protein, mouse); 0 (Tumor Suppressor Proteins); 128559-51-3 (RAG-1 protein); EC 2.1.1.319 (Prmt1 protein, mouse); EC 2.1.1.319 (Protein-Arginine N-Methyltransferases); EC 2.7.11.22 (Cdk4 protein, mouse); EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3774


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[PMID]:28541529
[Au] Autor:Hsieh G; Bierman R; Szabo L; Lee AG; Freeman DE; Watson N; Sweet-Cordero EA; Salzman J
[Ad] Endereço:Stanford University, Department of Biochemistry, 279 Campus Drive, Stanford, CA 94305, USA.
[Ti] Título:Statistical algorithms improve accuracy of gene fusion detection.
[So] Source:Nucleic Acids Res;45(13):e126, 2017 Jul 27.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Gene fusions are known to play critical roles in tumor pathogenesis. Yet, sensitive and specific algorithms to detect gene fusions in cancer do not currently exist. In this paper, we present a new statistical algorithm, MACHETE (Mismatched Alignment CHimEra Tracking Engine), which achieves highly sensitive and specific detection of gene fusions from RNA-Seq data, including the highest Positive Predictive Value (PPV) compared to the current state-of-the-art, as assessed in simulated data. We show that the best performing published algorithms either find large numbers of fusions in negative control data or suffer from low sensitivity detecting known driving fusions in gold standard settings, such as EWSR1-FLI1. As proof of principle that MACHETE discovers novel gene fusions with high accuracy in vivo, we mined public data to discover and subsequently PCR validate novel gene fusions missed by other algorithms in the ovarian cancer cell line OVCAR3. These results highlight the gains in accuracy achieved by introducing statistical models into fusion detection, and pave the way for unbiased discovery of potentially driving and druggable gene fusions in primary tumors.
[Mh] Termos MeSH primário: Algoritmos
Fusão Gênica
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Linhagem Celular Tumoral
Simulação por Computador
Bases de Dados de Ácidos Nucleicos
Feminino
Proteínas de Fusão bcr-abl/genética
Genes abl
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Neoplasias/genética
Fusão Oncogênica
Proteínas de Fusão Oncogênicas/genética
Neoplasias Ovarianas/genética
Alinhamento de Sequência
Análise de Sequência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (Oncogene Proteins, Fusion); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx453


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[PMID]:28504724
[Au] Autor:Giustacchini A; Thongjuea S; Barkas N; Woll PS; Povinelli BJ; Booth CAG; Sopp P; Norfo R; Rodriguez-Meira A; Ashley N; Jamieson L; Vyas P; Anderson K; Segerstolpe Å; Qian H; Olsson-Strömberg U; Mustjoki S; Sandberg R; Jacobsen SEW; Mead AJ
[Ad] Endereço:MRC Molecular Hematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
[Ti] Título:Single-cell transcriptomics uncovers distinct molecular signatures of stem cells in chronic myeloid leukemia.
[So] Source:Nat Med;23(6):692-702, 2017 Jun.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent advances in single-cell transcriptomics are ideally placed to unravel intratumoral heterogeneity and selective resistance of cancer stem cell (SC) subpopulations to molecularly targeted cancer therapies. However, current single-cell RNA-sequencing approaches lack the sensitivity required to reliably detect somatic mutations. We developed a method that combines high-sensitivity mutation detection with whole-transcriptome analysis of the same single cell. We applied this technique to analyze more than 2,000 SCs from patients with chronic myeloid leukemia (CML) throughout the disease course, revealing heterogeneity of CML-SCs, including the identification of a subgroup of CML-SCs with a distinct molecular signature that selectively persisted during prolonged therapy. Analysis of nonleukemic SCs from patients with CML also provided new insights into cell-extrinsic disruption of hematopoiesis in CML associated with clinical outcome. Furthermore, we used this single-cell approach to identify a blast-crisis-specific SC population, which was also present in a subclone of CML-SCs during the chronic phase in a patient who subsequently developed blast crisis. This approach, which might be broadly applied to any malignancy, illustrates how single-cell analysis can identify subpopulations of therapy-resistant SCs that are not apparent through cell-population analysis.
[Mh] Termos MeSH primário: Crise Blástica/genética
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Células-Tronco Neoplásicas/metabolismo
Análise de Célula Única
[Mh] Termos MeSH secundário: Adulto
Idoso
Imunoprecipitação da Cromatina
Subunidade alfa 2 de Fator de Ligação ao Core/genética
Feminino
Citometria de Fluxo
Biblioteca Gênica
Genes abl/genética
Seres Humanos
Hibridização in Situ Fluorescente
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
Masculino
Meia-Idade
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Análise de Sequência de DNA
Análise de Sequência de RNA
Transcriptoma
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 2 Subunit); 0 (RUNX1 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4336


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[PMID]:28502113
[Au] Autor:Dong Y; Wu C; Zhao X; Zhang P; Zhang H; Zheng M; Li S; Jiao J; Yu X; Lv Z; Ji Y
[Ad] Endereço:Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Centre, Xi'an, Shaanxi, China.
[Ti] Título:Epigenetic modifications of the V region after DJ recombination in Pro-B cells.
[So] Source:Immunology;152(2):218-231, 2017 Oct.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The variable region of murine immunoglobulin heavy chain (Igh) is assembled by sequential D -J and V -DJ recombination. The accessibility of the Igh locus determines the order of rearrangement. Because of the large number of V genes and the lack of a suitable model, the epigenetic modifications of V genes after DJ recombination have not previously been characterized. Here, we employed two v-Abl pro-B cell lines, in which the Igh locus is in germline and DJ -recombined configurations, respectively. The DJ junction displays the characteristics of a recombination centre, such as high levels of activation-associated histone modifications and recombination-activating gene protein (RAG) binding in DJ -rearranged pro-B cells, which extend the recombination centre model proposed for the germline Igh locus. The different domains of the V region have distinct epigenetic characteristics after DJ recombination. Distal V genes have higher levels of active histone modifications, germline transcription and Pax5 binding, and good quality recombination signal sequences. Proximal V genes are relatively close to the DJ recombination centre, which partially compensates for the low levels of the above active epigenetic modifications. DJ recombination centre might serve as a cis-acting element to regulate the accessibility of the V region. Furthermore, we demonstrate that RAG weakly binds to functional V genes, which is the first detailed assessment of RAG dynamic binding to V genes. We provide a way for V -DJ recombination in which the V gene is brought into close proximity with the DJ recombination centre for RAG binding by a Pax5-dependent chromosomal compaction event, and held in this position for subsequent cleavage and V -DJ joining.
[Mh] Termos MeSH primário: Epigênese Genética
Rearranjo Gênico do Linfócito B
Genes de Cadeia Pesada de Imunoglobulina
Região Variável de Imunoglobulina/genética
Células Precursoras de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Acetilação
Animais
Linhagem Celular Transformada
Imunoprecipitação da Cromatina
Proteínas de Ligação a DNA/imunologia
Proteínas de Ligação a DNA/metabolismo
Genes abl
Células HEK293
Histonas/metabolismo
Proteínas de Homeodomínio/imunologia
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Região de Junção de Imunoglobulinas/genética
Região de Junção de Imunoglobulinas/imunologia
Região Variável de Imunoglobulina/imunologia
Região Variável de Imunoglobulina/metabolismo
Metilação
Camundongos
Camundongos Endogâmicos C57BL
Fator de Transcrição PAX5/genética
Fator de Transcrição PAX5/metabolismo
Células Precursoras de Linfócitos B/metabolismo
Ligação Proteica
Processamento de Proteína Pós-Traducional
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Histones); 0 (Homeodomain Proteins); 0 (Immunoglobulin Joining Region); 0 (Immunoglobulin Variable Region); 0 (PAX5 Transcription Factor); 0 (Pax5 protein, mouse); 0 (Rag2 protein, mouse); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170515
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12758


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[PMID]:28481221
[Au] Autor:Nieborowska-Skorska M; Sullivan K; Dasgupta Y; Podszywalow-Bartnicka P; Hoser G; Maifrede S; Martinez E; Di Marcantonio D; Bolton-Gillespie E; Cramer-Morales K; Lee J; Li M; Slupianek A; Gritsyuk D; Cerny-Reiterer S; Seferynska I; Stoklosa T; Bullinger L; Zhao H; Gorbunova V; Piwocka K; Valent P; Civin CI; Muschen M; Dick JE; Wang JC; Bhatia S; Bhatia R; Eppert K; Minden MD; Sykes SM; Skorski T
[Ad] Endereço:Temple University Lewis Katz School of Medicine, Department of Microbiology and Immunology and Fels Institute for Cancer Research & Molecular Biology, Philadelphia, Pennsylvania, USA.
[Ti] Título:Gene expression and mutation-guided synthetic lethality eradicates proliferating and quiescent leukemia cells.
[So] Source:J Clin Invest;127(6):2392-2406, 2017 Jun 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quiescent and proliferating leukemia cells accumulate highly lethal DNA double-strand breaks that are repaired by 2 major mechanisms: BRCA-dependent homologous recombination and DNA-dependent protein kinase-mediated (DNA-PK-mediated) nonhomologous end-joining, whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1 (PARP1) serve as backups. Here we have designed a personalized medicine approach called gene expression and mutation analysis (GEMA) to identify BRCA- and DNA-PK-deficient leukemias either directly, using reverse transcription-quantitative PCR, microarrays, and flow cytometry, or indirectly, by the presence of oncogenes such as BCR-ABL1. DNA-PK-deficient quiescent leukemia cells and BRCA/DNA-PK-deficient proliferating leukemia cells were sensitive to PARP1 inhibitors that were administered alone or in combination with current antileukemic drugs. In conclusion, GEMA-guided targeting of PARP1 resulted in dual cellular synthetic lethality in quiescent and proliferating immature leukemia cells, and is thus a potential approach to eradicate leukemia stem and progenitor cells that are responsible for initiation and manifestation of the disease. Further, an analysis of The Cancer Genome Atlas database indicated that this personalized medicine approach could also be applied to treat numerous solid tumors from individual patients.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Proliferação Celular
Leucemia/genética
Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Transformação Celular Neoplásica
Cricetinae
Quebras de DNA de Cadeia Dupla
Reparo do DNA por Junção de Extremidades
Genes BRCA1
Genes BRCA2
Genes Letais
Genes abl
Seres Humanos
Leucemia/tratamento farmacológico
Camundongos
Camundongos Endogâmicos NOD
Camundongos Knockout
Camundongos SCID
Células-Tronco Embrionárias Murinas/fisiologia
Ftalazinas/farmacologia
Piperazinas/farmacologia
Transcriptoma
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phthalazines); 0 (Piperazines); 0 (Poly(ADP-ribose) Polymerase Inhibitors); 9QHX048FRV (talazoparib); WOH1JD9AR8 (olaparib)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


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[PMID]:28356344
[Au] Autor:Chen TH; Chen CY; Wen HC; Chang CC; Wang HD; Chuu CP; Chang CH
[Ad] Endereço:Department of Life Science, National Tsing Hua University, Hsin-Chu, Taiwan, China.
[Ti] Título:YAP promotes myogenic differentiation the MEK5-ERK5 pathway.
[So] Source:FASEB J;31(7):2963-2972, 2017 Jul.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Yes-associated protein (YAP) is a transcriptional coactivator in the Hippo pathway that regulates cell proliferation, differentiation, and apoptosis. The MEK5/ERK5 MAPK cascade is essential for the early step of myogenesis. In this study, we generated C2C12 stable cell lines that expressed YAP (C2C12-YAP cells) and found that ERK5 and MEK5 were activated in C2C12-YAP cells compared with control C2C12 (C2C12-vector) cells. C2C12-YAP stable cells also differentiated into myotubes better than C2C12-vector cells, and expressed elevated levels of myogenin, a transcription factor that regulates myogenesis, as well as elevated levels of myosin heavy chain, a skeletal muscle marker. Western blot analysis revealed that Src and c-Abl (Abelson murine leukemia viral oncogene homolog 1) activation were enhanced in C2C12-YAP cells. Conversely, treatment of inhibitors of c-Abl, Src, or MEK5 inhibited activation of MEK5 and ERK5 and myogenesis of C2C12 myoblasts. Specific interactions between YAP and proteins in the ERK5 pathway, such as MEK kinase 3 (MEKK3) and ERK5, were illustrated by coimmunoprecipitation experiments. MEKK3 contains the PPGY motif (aa 178-181), which may interact with YAP. Site-directed mutagenesis experiments revealed that expression of MEKK3 Y181F mutant inhibited MEK5/ERK5 activation and myogenic differentiation. These results suggest that YAP promotes muscle differentiation by activating the Abl/Src/MEKK3/MEK5/ERK5 kinase cascade.-Chen, T.-H., Chen, C.-Y., Wen, H.-C., Chang, C.-C., Wang, H.-D., Chuu, C.-P., Chang, C.-H. YAP promotes myogenic differentiation the MEK5-ERK5 pathway.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Regulação da Expressão Gênica/fisiologia
MAP Quinase Quinase 5/metabolismo
Proteína Quinase 7 Ativada por Mitógeno/metabolismo
Fosfoproteínas/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Animais
Diferenciação Celular
Linhagem Celular
Citoplasma
Genes abl
MAP Quinase Quinase 5/genética
MAP Quinase Quinase Quinase 3/genética
MAP Quinase Quinase Quinase 3/metabolismo
Camundongos
Proteína Quinase 7 Ativada por Mitógeno/genética
Desenvolvimento Muscular/fisiologia
Fibras Musculares Esqueléticas/metabolismo
Fosfoproteínas/genética
Transporte Proteico
Quinases da Família src
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Phosphoproteins); 0 (Yap protein, mouse); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 7); EC 2.7.11.25 (MAP Kinase Kinase Kinase 3); EC 2.7.11.25 (Map3k3 protein, mouse); EC 2.7.12.2 (MAP Kinase Kinase 5); EC 2.7.12.2 (Map2k5 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601090R


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[PMID]:28319094
[Au] Autor:Kesarwani M; Kincaid Z; Gomaa A; Huber E; Rohrabaugh S; Siddiqui Z; Bouso MF; Latif T; Xu M; Komurov K; Mulloy JC; Cancelas JA; Grimes HL; Azam M
[Ad] Endereço:Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
[Ti] Título:Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
[So] Source:Nat Med;23(4):472-482, 2017 Apr.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tyrosine-kinase inhibitor (TKI) therapy for human cancers is not curative, and relapse occurs owing to the continued presence of tumor cells, referred to as minimal residual disease (MRD). The survival of MRD stem or progenitor cells in the absence of oncogenic kinase signaling, a phenomenon referred to as intrinsic resistance, depends on diverse growth factors. Here we report that oncogenic kinase and growth-factor signaling converge to induce the expression of the signaling proteins FBJ osteosarcoma oncogene (c-FOS, encoded by Fos) and dual-specificity phosphatase 1 (DUSP1). Genetic deletion of Fos and Dusp1 suppressed tumor growth in a BCR-ABL fusion protein kinase-induced mouse model of chronic myeloid leukemia (CML). Pharmacological inhibition of c-FOS, DUSP1 and BCR-ABL eradicated MRD in multiple in vivo models, as well as in mice xenotransplanted with patient-derived primary CML cells. Growth-factor signaling also conferred TKI resistance and induced FOS and DUSP1 expression in tumor cells modeling other types of kinase-driven leukemias. Our data demonstrate that c-FOS and DUSP1 expression levels determine the threshold of TKI efficacy, such that growth-factor-induced expression of c-FOS and DUSP1 confers intrinsic resistance to TKI therapy in a wide-ranging set of leukemias, and might represent a unifying Achilles' heel of kinase-driven cancers.
[Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos/genética
Fosfatase 1 de Especificidade Dupla/genética
Genes abl/genética
Mesilato de Imatinib/farmacologia
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-fos/genética
[Mh] Termos MeSH secundário: Adulto
Animais
Apoptose/efeitos dos fármacos
Western Blotting
Proliferação Celular/efeitos dos fármacos
Feminino
Citometria de Fluxo
Perfilação da Expressão Gênica
Seres Humanos
Mesilato de Imatinib/uso terapêutico
Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Meia-Idade
Transplante de Neoplasias
Neoplasia Residual
Neoplasias Experimentais/genética
Inibidores de Proteínas Quinases/uso terapêutico
Reação em Cadeia da Polimerase em Tempo Real
Ensaio Tumoral de Célula-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-fos); 8A1O1M485B (Imatinib Mesylate); EC 3.1.3.48 (Dual Specificity Phosphatase 1); EC 3.1.3.48 (Dusp1 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170321
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4310


  9 / 1185 MEDLINE  
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[PMID]:28196667
[Au] Autor:Wolczyk M; Podszywalow-Bartnicka P; Bugajski L; Piwocka K
[Ad] Endereço:Laboratory of Cytometry, Nencki Institute of Experimental Biology, 3 Pasteur Street, 02-093 Warsaw, Poland. Electronic address: m.wolczyk@nencki.gov.pl.
[Ti] Título:Stress granules assembly affects detection of mRNA in living cells by the NanoFlares; an important aspect of the technology.
[So] Source:Biochim Biophys Acta;1861(5 Pt A):1024-1035, 2017 05.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The recently announced new methodologies to detect mRNA molecules in single cells offer opportunities for research, medicine and molecular diagnostics. The NanoFlare RNA Detection Probes are tools for characterizing RNA content (not localization) using fluorescence-based approaches in living cells. Combined with flow cytometry, NanoFlares have expanded the available possibilities of quantitative analysis of mRNA level in a single cell. Herein we present that in some cases, the specific NanoFlare probes (SmartFlares) detect different amounts of mRNA compared to qPCR. Using the previously published model, in which we studied influence of BCR-ABL oncogene on BRCA1 mRNA translation, we found that the NanoFlare-mediated measurement of mRNA was affected by the assembly of stress granules, structures which store mRNA in complexes with RNA binding proteins. With the usage of chemical compounds we confirmed that under conditions supporting assembly of stress granules, the detection of mRNAs by these probes was decreased, whereas disassembly resulted in the increased mRNAs detection. Altogether, we showed that assembly of stress granules could interfere with mRNA accessibility to the NanoFlare RNA Detection Probes, indicating that the SmartFlares could recognize only the translationally active pool of mRNA, contrary to qPCR. This can significantly influence the quality of obtained data and should be taken into consideration while planning the analysis of mRNA markers using NanoFlares.
[Mh] Termos MeSH primário: Grânulos Citoplasmáticos/fisiologia
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína BRCA1/metabolismo
Linhagem Celular
Fluorescência
Genes abl/genética
Camundongos
Biossíntese de Proteínas/fisiologia
RNA/metabolismo
Proteínas de Ligação a RNA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BRCA1 Protein); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 63231-63-0 (RNA)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE


  10 / 1185 MEDLINE  
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[PMID]:27630163
[Au] Autor:Meng J; Jiang JJ; Atsumi T; Bando H; Okuyama Y; Sabharwal L; Nakagawa I; Higuchi H; Ota M; Okawara M; Ishitani R; Nureki O; Higo D; Arima Y; Ogura H; Kamimura D; Murakami M
[Ad] Endereço:Division of Molecular Neuroimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo 080-0615, Japan.
[Ti] Título:Breakpoint Cluster Region-Mediated Inflammation Is Dependent on Casein Kinase II.
[So] Source:J Immunol;197(8):3111-3119, 2016 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The breakpoint cluster region (BCR) is known as a kinase and cause of leukemia upon fusing to Abl kinase. In this study, we demonstrate that BCR associated with the α subunit of casein kinase II (CK2α), rather than BCR itself, is required for inflammation development. We found that BCR knockdown inhibited NF-κB activation in vitro and in vivo. Computer simulation, however, suggested that the putative BCR kinase domain has an unstable structure with minimal enzymatic activity. Liquid chromatography-tandem mass spectrometry analysis showed that CK2α associated with BCR. We found the BCR functions are mediated by CK2α. Indeed, CK2α associated with adaptor molecules of TNF-αR and phosphorylated BCR at Y177 to establish a p65 binding site after TNF-α stimulation. Notably, p65 S529 phosphorylation by CK2α creates a p300 binding site and increased p65-mediated transcription followed by inflammation development in vivo. These results suggest that BCR-mediated inflammation is dependent on CK2α, and the BCR-CK2α complex could be a novel therapeutic target for various inflammatory diseases.
[Mh] Termos MeSH primário: Artrite/genética
Caseína Quinase II/metabolismo
Proteínas de Fusão bcr-abl/metabolismo
Cromossomo Filadélfia
Proteínas Proto-Oncogênicas c-bcr/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/genética
Linhagem Celular
Cromatografia Líquida
Proteínas de Fusão bcr-abl/genética
Genes abl/genética
Seres Humanos
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/metabolismo
Proteínas Proto-Oncogênicas c-bcr/genética
RNA Interferente Pequeno/genética
Espectrometria de Massas em Tandem
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Tumor Necrosis Factor-alpha); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 2.7.11.1 (Casein Kinase II); EC 2.7.11.1 (Proto-Oncogene Proteins c-bcr)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE



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