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[PMID]:29430664
[Au] Autor:Budzynska PM; Kyläniemi MK; Lassila O; Nera KP; Alinikula J
[Ad] Endereço:Department of Medical Microbiology and Immunology, Institute of Biomedicine, University of Turku, Turku, Finland.
[Ti] Título:BLIMP-1 is insufficient to induce antibody secretion in the absence of IRF4 in DT40 cells.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Differentiation of B cells into antibody-secreting cells (ASCs), plasmablasts and plasma cells is regulated by a network of transcription factors. Within this network, factors including PAX5 and BCL6 prevent ASC differentiation and maintain the B cell phenotype. In contrast, BLIMP-1 and high IRF4 expression promote plasma cell differentiation. BLIMP-1 is thought to induce immunoglobulin secretion, whereas IRF4 is needed for the survival of ASCs. The role of IRF4 in the regulation of antibody secretion has remained controversial. To study the role of IRF4 in the regulation of antibody secretion, we have created a double knockout (DKO) DT40 B cell line deficient in both IRF4 and BCL6. Although BCL6-deficient DT40 B cell line had upregulated BLIMP-1 expression and secreted antibodies, the DKO cell line did not. Even enforced BLIMP-1 expression in DKO cells or IRF4-deficient cells could not induce IgM secretion while in WT DT40 cells, it could. However, enforced IRF4 expression in DKO cells induced strong IgM secretion. Our findings support a model where IRF4 expression in addition to BLIMP-1 expression is required to induce robust antibody secretion.
[Mh] Termos MeSH primário: Anticorpos/imunologia
Formação de Anticorpos/genética
Proteínas Aviárias/genética
Linfócitos B/imunologia
Fatores Reguladores de Interferon/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Diferenciação Celular/imunologia
Linhagem Celular
Proliferação Celular
Galinhas
Técnicas de Inativação de Genes
Imunoglobulina M/biossíntese
Imunoglobulina M/imunologia
Fator de Transcrição PAX5/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/imunologia
Proteínas Proto-Oncogênicas c-bcl-6/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Avian Proteins); 0 (IRF4 protein, Gallus gallus); 0 (Immunoglobulin M); 0 (Interferon Regulatory Factors); 0 (PAX5 Transcription Factor); 0 (Proto-Oncogene Proteins c-bcl-6); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12646


  2 / 759 MEDLINE  
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[PMID]:29325247
[Au] Autor:Zhang XY; Ma ZP; Cui WL; Pang XL; Chen R; Wang L; Zhang W; Li XX
[Ad] Endereço:Department of Pathology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
[Ti] Título:[Impact of PRDM1 gene inactivation on C-MYC regulation in diffuse large B-cell lymphoma].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):25-31, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the role of PRDM1 gene inactivaion in the regulation of C-MYC in diffuse large B-cell lymphoma (DLBCL), and to explore the correlation of its immunophenotype and prognosis. 100 cases paraffin-embedded DLBCL tissues were collected from January 2009 to December 2015 at the First Affiliated Hospital of Xinjiang Medical University along with 20 cases of reactive proliferative lymph nodes as control. Immunohistochemical methods were used to detect the expression of CD20, CD10, MUM1, Ki-67, bcl-6, PRDM1/Blimp1, C-MYC and PAX5 protein. The tumors were classified into two subtypes according to Hans classification.The expression of PRDM1 and C-MYC gene in tumor group and control group was detected by reverse transcription PCR (RT-PCR) and the relationship between PRDM1 and C-MYC gene was analyzed.OCI-LY1 (GCB subtype) and OCI-LY3 (non-GCB subtype) cell lines were transfected with small interfering RNA by cationic liposome reagent transfection, and the expression of C-MYC in the transfected cell lines was detected by RT-PCR and Western blot. The Kaplan-Meier method was used to analyze the prognostic significance of PRDM1/Blimp1 and C-MYC at protein and mRNA levels. There were 27 cases of GCB subtype and 73 cases of non-GCB subtype according to Hans classification. The positive expression of Blimp1 in DLBCL group and proliferative lymph nodes in control group was seen in 26(26.0%) and 20 cases(100%), respectively. There were 58 cases with high expression of PRDM1 at mRNA level, including 22 cases of GCB subtype and 36 cases non-GCB subtype, and the difference was statistically significant ( =0.004). There were differences in PRDM1 gene expression between the two immunological subtypes, serum lactate dehydrogenase (serum LDH) level, presence of B symptoms, tumor primary sites and other clinical pathological parameters, while C-MYC expression was different in gender, IPI score, and serum LDH levels. Upon PRDM1/Blimp1 gene silencing in the two cell lines, C-MYC protein and gene expression were up-regulated in the transfection group, compared with the blank control group and negative control group by reverse transcription PCR and Western blot analyses. Moreover, PRDM1 expression was significantly associated with C-MYC(χ(2)=7.648, =0.006) at mRNA level. The up-regulation of C-MYC gene expression induced by PRDM1 inactivation in DLBCL may play an important role for the development of DLBCL.PRDM1 protein and mRNA are associated with immunophenotyping and PRDM1 mRNA is a marker of poor prognosis.
[Mh] Termos MeSH primário: Inativação Gênica
Genes myc
Linfoma Difuso de Grandes Células B/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
[Mh] Termos MeSH secundário: Antígenos CD20/metabolismo
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imunofenotipagem
Linfonodos/patologia
Linfoma Difuso de Grandes Células B/patologia
Fator de Transcrição PAX5/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
RNA Mensageiro/metabolismo
Proteínas Repressoras/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD20); 0 (PAX5 Transcription Factor); 0 (PAX5 protein, human); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Messenger); 0 (Repressor Proteins); 138415-26-6 (PRDM1 protein, human); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.006


  3 / 759 MEDLINE  
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[PMID]:28655536
[Au] Autor:Chan LN; Müschen M
[Ad] Endereço:Department of Systems Biology, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Pasadena, CA. Electronic address: lachan@coh.org.
[Ti] Título:B-cell identity as a metabolic barrier against malignant transformation.
[So] Source:Exp Hematol;53:1-6, 2017 Sep.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:B-lineage and myeloid leukemia cells are often transformed by the same oncogenes, but have different biological and clinical characteristics. Although B-lineage acute lymphoblastic leukemia (B-ALL) cells are characterized by a state of chronic energy deficit, myeloid leukemia cells show abundant energy reserve. Interestingly, fasting has been demonstrated to inhibit selectively the development of B-ALL but not myeloid leukemia, further suggesting that lineage identity may be linked to divergent metabolic states in hematopoietic malignancies. The B-lymphoid transcription factors IKZF1, EBF1, and PAX5 are essential for early B-cell development and commitment to B-cell identity. However, in >80% of human pre-B-ALL cases, the leukemic clones harbor genetic lesions of these transcription factors. The significance of these defects has only recently been investigated. Here, we discuss the unexpected function of a B-lymphoid transcriptional program as a metabolic barrier against malignant transformation of B-cell precursor cells. The metabolic gatekeeper function of B-lymphoid transcription factors may force silent preleukemic clones carrying potentially oncogenic lesions to remain in a latent state. In addition, this program sets the threshold for responses to glucocorticoids in pre-B-ALL. Finally, the link between the tumor-suppressor and metabolic functions of B-lymphoid transcription factors is matched by observations in clinical trials: obesity and hyperglycemia are associated with poor clinical outcome in patients with pre-B-ALL.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Transformação Celular Neoplásica
Leucemia-Linfoma Linfoblástico de Células Precursoras B/etiologia
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Metabolismo Energético
Proteína Forkhead Box O1/fisiologia
Seres Humanos
Fator de Transcrição Ikaros/fisiologia
Camundongos
Obesidade/complicações
Fator de Transcrição PAX5/fisiologia
Fosfatidilinositol 3-Quinases/fisiologia
Proteínas Proto-Oncogênicas c-akt/fisiologia
Receptores para Leptina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Forkhead Box Protein O1); 0 (IKZF1 protein, human); 0 (PAX5 Transcription Factor); 0 (Receptors, Leptin); 148971-36-2 (Ikaros Transcription Factor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE


  4 / 759 MEDLINE  
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[PMID]:28533268
[Au] Autor:Solanki A; Lau CI; Saldaña JI; Ross S; Crompton T
[Ad] Endereço:Great Ormond Street Institute of Child Health, University College London, London, England, UK.
[Ti] Título:The transcription factor Gli3 promotes B cell development in fetal liver through repression of Shh.
[So] Source:J Exp Med;214(7):2041-2058, 2017 Jul 03.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Before birth, B cells develop in the fetal liver (FL). In this study, we show that Gli3 activity in the FL stroma is required for B cell development. In the Gli3-deficient FL, B cell development was reduced at multiple stages, whereas the Sonic hedgehog (Hh [Shh])-deficient FL showed increased B cell development, and Gli3 functioned to repress transcription. Use of a transgenic Hh-reporter mouse showed that Shh signals directly to developing B cells and that Hh pathway activation was increased in developing B cells from Gli3-deficient FLs. RNA sequencing confirmed that Hh-mediated transcription is increased in B-lineage cells from Gli3-deficient FL and showed that these cells expressed reduced levels of B-lineage transcription factors and B cell receptor (BCR)/pre-BCR-signaling genes. Expression of the master regulators of B cell development Ebf1 and Pax5 was reduced in developing B cells from Gli3-deficient FL but increased in Shh-deficient FL, and in vitro Shh treatment or neutralization reduced or increased their expression, respectively.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Proteínas Hedgehog/genética
Fatores de Transcrição Kruppel-Like/genética
Fígado/metabolismo
Proteínas do Tecido Nervoso/genética
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula/genética
Citometria de Fluxo
Perfilação da Expressão Gênica/métodos
Fígado/embriologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Fator de Transcrição PAX5/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/genética
Transativadores/genética
Proteína Gli3 com Dedos de Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ebf1 protein, mouse); 0 (Gli3 protein, mouse); 0 (Hedgehog Proteins); 0 (Kruppel-Like Transcription Factors); 0 (Nerve Tissue Proteins); 0 (PAX5 Transcription Factor); 0 (Pax5 protein, mouse); 0 (Trans-Activators); 0 (Zinc Finger Protein Gli3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160852


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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]:28418282
[Au] Autor:Rozenvald IB; Richardson MD; Brock L; Maiese RL
[Ti] Título:Immunohistochemical Detection of Hairy Cell Leukemia in Paraffin Sections: The Role of Pax5 and CD103 Double Staining to Improve Specificity and Sensitivity.
[So] Source:Arch Pathol Lab Med;141(6):837-840, 2017 Jun.
[Is] ISSN:1543-2165
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT: - In hematopathology practice, abnormal expression of CD103 on B cells is detected by flow cytometry in hairy cell leukemia (HCL) and, in combination with other phenotypic and morphologic findings, provides diagnostic specificity and sensitivity. Immunostaining on paraffin sections makes it possible to perform immunophenotyping in situ. However, normal bone marrow contains CD103-positive cells, which are not B cells, making it difficult to be certain about low-level involvement by HCL. OBJECTIVE: - To develop dual immunostaining for confirmation that CD103 is expressed in B cells, which may be highly desirable in assessing low-level involvement by HCL. DESIGN: - We developed a dual immunostaining approach using a B-cell marker, Pax5, expressed in the nucleus, in combination with a membrane marker, CD103. RESULTS: - We analyzed 6 HCLs, 7 marginal zone lymphomas, 12 lymphoplasmacytic lymphomas, 7 follicular lymphomas, 5 chronic lymphocytic leukemias, 5 mantle cell lymphomas, 1 multiple myeloma (lymphocytic variant), and 3 bone marrows not involved by any B-cell neoplasm. Our dual staining approach confirmed that only the neoplastic cells of HCL were positive for both CD103 and Pax5. CONCLUSIONS: - This dual-staining method is particularly helpful in cases with low-level involvement by HCL and can be used for determining minimal residual disease after treatment.
[Mh] Termos MeSH primário: Antígenos CD/análise
Biomarcadores Tumorais/análise
Cadeias alfa de Integrinas/análise
Leucemia de Células Pilosas/diagnóstico
Fator de Transcrição PAX5/análise
[Mh] Termos MeSH secundário: Medula Óssea/metabolismo
Medula Óssea/patologia
Seres Humanos
Imuno-Histoquímica/métodos
Imunofenotipagem/métodos
Leucemia de Células Pilosas/metabolismo
Leucemia de Células Pilosas/patologia
Leucemia Linfocítica Crônica de Células B/diagnóstico
Leucemia Linfocítica Crônica de Células B/metabolismo
Leucemia Linfocítica Crônica de Células B/patologia
Linfoma não Hodgkin/diagnóstico
Linfoma não Hodgkin/metabolismo
Linfoma não Hodgkin/patologia
Mieloma Múltiplo/diagnóstico
Mieloma Múltiplo/metabolismo
Mieloma Múltiplo/patologia
Neoplasia Residual
Inclusão em Parafina
Sensibilidade e Especificidade
Coloração e Rotulagem/métodos
Macroglobulinemia de Waldenstrom/diagnóstico
Macroglobulinemia de Waldenstrom/metabolismo
Macroglobulinemia de Waldenstrom/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers, Tumor); 0 (Integrin alpha Chains); 0 (PAX5 Transcription Factor); 0 (PAX5 protein, human); 0 (alpha E integrins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.5858/arpa.2016-0215-OA


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[PMID]:28371317
[Au] Autor:Schmäh J; Fedders B; Panzer-Grümayer R; Fischer S; Zimmermann M; Dagdan E; Bens S; Schewe D; Moericke A; Alten J; Bleckmann K; Siebert R; Schrappe M; Stanulla M; Cario G
[Ad] Endereço:Department of Pediatrics, University Medical Center Schleswig-Holstein, Kiel, Germany.
[Ti] Título:Molecular characterization of acute lymphoblastic leukemia with high CRLF2 gene expression in childhood.
[So] Source:Pediatr Blood Cancer;64(10), 2017 Oct.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A high-level expression of the CRLF2 gene is frequent in precursor B-cell acute lymphoblastic leukemia (pB-ALL) and can be caused by different genetic aberrations. The presence of the most frequent alteration, the P2RY8/CRLF2 fusion, was shown to be associated with a high relapse incidence in children treated according to ALL-Berlin-Frankfurt-Münster (BFM) protocols, which is poorly understood. Moreover, the frequency of other alterations has not been systematically analyzed yet. PROCEDURE: CRLF2 mRNA expression and potential genetic aberrations causing a CRLF2 high expression were prospectively assessed in 1,105 patients treated according to the Associazione Italiana Ematologia Oncologia Pediatrica (AIEOP)-BFM ALL 2009 protocol. Additionally, we determined copy number alterations in selected B-cell differentiation genes for all CRLF2 high-expressing pB-ALL cases, as well as JAK2 and CRLF2 mutations. RESULTS: A CRLF2 high expression was detected in 26/178 (15%) T-cell acute lymphoblastic leukemia (T-ALL) cases, 21 of them (81%) had been stratified as high-risk patients by treatment response. In pB-ALL, a CRLF2 high expression was determined in 91/927 (10%) cases; the P2RY8/CRLF2 rearrangement in 44/91 (48%) of them, supernumerary copies of CRLF2 in 18/91 (20%), and, notably, the IGH/CRLF2 translocation was detected in 16/91 (18%). Remarkably, 7 of 16 (44%) patients with IGH/CRLF2 translocation had already relapsed. P2RY8/CRLF2- and IGH/CRLF2-positive samples (70 and 94%, respectively) were characterized by a high frequency of additional deletions in B-cell differentiation genes such as IKZF1 or PAX5. CONCLUSION: Our data suggest that this high frequency of genetic aberrations in the context of a high CRLF2 expression could contribute to the high risk of relapse in P2RY8/CRLF2- and IGH/CRLF2-positive ALL.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Regulação Leucêmica da Expressão Gênica/efeitos dos fármacos
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras/metabolismo
Receptores de Citocinas/biossíntese
[Mh] Termos MeSH secundário: Adolescente
Asparaginase/administração & dosagem
Criança
Pré-Escolar
Daunorrubicina/administração & dosagem
Feminino
Rearranjo Gênico
Seres Humanos
Fator de Transcrição Ikaros/biossíntese
Fator de Transcrição Ikaros/genética
Lactente
Masculino
Proteínas de Fusão Oncogênicas/biossíntese
Proteínas de Fusão Oncogênicas/genética
Fator de Transcrição PAX5/biossíntese
Fator de Transcrição PAX5/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Prednisona/administração & dosagem
Receptores de Citocinas/genética
Receptores Purinérgicos P2Y/biossíntese
Receptores Purinérgicos P2Y/genética
Vincristina/administração & dosagem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (CRLF2 protein, human); 0 (IKZF1 protein, human); 0 (Oncogene Proteins, Fusion); 0 (P2RY8 protein, human); 0 (PAX5 Transcription Factor); 0 (PAX5 protein, human); 0 (Receptors, Cytokine); 0 (Receptors, Purinergic P2Y); 148971-36-2 (Ikaros Transcription Factor); 5J49Q6B70F (Vincristine); EC 3.5.1.1 (Asparaginase); VB0R961HZT (Prednisone); ZS7284E0ZP (Daunorubicin)
[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:170404
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26539


  8 / 759 MEDLINE  
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[PMID]:28369050
[Au] Autor:Katerndahl CDS; Heltemes-Harris LM; Willette MJL; Henzler CM; Frietze S; Yang R; Schjerven H; Silverstein KAT; Ramsey LB; Hubbard G; Wells AD; Kuiper RP; Scheijen B; van Leeuwen FN; Müschen M; Kornblau SM; Farrar MA
[Ad] Endereço:Department of Laboratory Medicine and Pathology, Center for Immunology, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.
[Ti] Título:Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival.
[So] Source:Nat Immunol;18(6):694-704, 2017 Jun.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor STAT5 has a critical role in B cell acute lymphoblastic leukemia (B-ALL). How STAT5 mediates this effect is unclear. Here we found that activation of STAT5 worked together with defects in signaling components of the precursor to the B cell antigen receptor (pre-BCR), including defects in BLNK, BTK, PKCß, NF-κB1 and IKAROS, to initiate B-ALL. STAT5 antagonized the transcription factors NF-κB and IKAROS by opposing regulation of shared target genes. Super-enhancers showed enrichment for STAT5 binding and were associated with an opposing network of transcription factors, including PAX5, EBF1, PU.1, IRF4 and IKAROS. Patients with a high ratio of active STAT5 to NF-κB or IKAROS had more-aggressive disease. Our studies indicate that an imbalance of two opposing transcriptional programs drives B-ALL and suggest that restoring the balance of these pathways might inhibit B-ALL.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Linfócitos B
Regulação Neoplásica da Expressão Gênica
Fator de Transcrição Ikaros/genética
Receptores de Células Precursoras de Linfócitos B/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Fator de Transcrição STAT5/metabolismo
[Mh] Termos MeSH secundário: Animais
Imunoprecipitação da Cromatina
Citometria de Fluxo
Seres Humanos
Fatores Reguladores de Interferon/genética
Camundongos
Reação em Cadeia da Polimerase Multiplex
Subunidade p50 de NF-kappa B/genética
Fator de Transcrição PAX5/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras/mortalidade
Prognóstico
Proteína Quinase C beta/genética
Proteínas Tirosina Quinases/genética
Proteínas Proto-Oncogênicas/genética
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Taxa de Sobrevida
Transativadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (B cell linker protein); 0 (Ebf1 protein, mouse); 0 (IKZF1 protein, human); 0 (Interferon Regulatory Factors); 0 (NF-kappa B p50 Subunit); 0 (PAX5 Transcription Factor); 0 (Pax5 protein, mouse); 0 (Pre-B Cell Receptors); 0 (Proto-Oncogene Proteins); 0 (STAT5 Transcription Factor); 0 (Trans-Activators); 0 (Zfpn1a1 protein, mouse); 0 (interferon regulatory factor-4); 0 (proto-oncogene protein Spi-1); 147257-52-1 (Nfkb1 protein, mouse); 148971-36-2 (Ikaros Transcription Factor); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.11.13 (Protein Kinase C beta); EC 2.7.11.13 (prkcb1 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3716


  9 / 759 MEDLINE  
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[PMID]:28316978
[Au] Autor:Gu J; Li T; Zhao L; Liang X; Fu X; Wang J; Shang Z; Huang W; Zhou J
[Ad] Endereço:Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Identification of Significant Pathways Induced by PAX5 Haploinsufficiency Based on Protein-Protein Interaction Networks and Cluster Analysis in Raji Cell Line.
[So] Source:Biomed Res Int;2017:5326370, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PAX5 encodes a transcription factor essential for B-cell differentiation, and PAX5 haploinsufficiency is involved in tumorigenesis. There were few studies on how PAX5 haploinsufficiency regulated genes expression to promote tumorigenesis. In this study, we constructed the cell model of PAX5 haploinsufficiency using gene editing technology in Raji cells, detected differentially expressed genes in PAX5 haploinsufficiency Raji cells, and used protein-protein interaction networks and cluster analysis to comprehensively investigate the cellular pathways involved in PAX5 haploinsufficiency. The clusters of gene transcription, inflammatory and immune response, and cancer pathways were identified as three important pathways associated with PAX5 haploinsufficiency in Raji cells. These changes hinted that the mechanism of PAX5 haploinsufficiency promoting tumorigenesis may be related to genomic instability, immune tolerance, and tumor pathways.
[Mh] Termos MeSH primário: Haploinsuficiência
Fator de Transcrição PAX5/genética
Mapeamento de Interação de Proteínas
[Mh] Termos MeSH secundário: Alelos
Motivos de Aminoácidos
Sistemas CRISPR-Cas
Carcinogênese
Linhagem Celular Tumoral
Análise por Conglomerados
Biologia Computacional
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Vetores Genéticos
Instabilidade Genômica
Células HEK293
Seres Humanos
Tolerância Imunológica
Inflamação
Mutação
Análise de Sequência com Séries de Oligonucleotídeos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PAX5 Transcription Factor); 0 (PAX5 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170321
[St] Status:MEDLINE
[do] DOI:10.1155/2017/5326370


  10 / 759 MEDLINE  
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[PMID]:28296741
[Au] Autor:Jiang C; Shi X; Fan C
[Ad] Endereço:Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.
[Ti] Título:A cyclin D1-positive diffuse large B-cell lymphoma of germinal center B-cell-like subtype in the right tonsil: A rare case report.
[So] Source:Medicine (Baltimore);96(11):e6311, 2017 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Cyclin D1-positive tumor cells are commonly found in mantle cell lymphoma but they are very rare in diffuse large B-cell lymphoma. CLINICAL FINDINGS/PATIENT CONCERNS: Here we present a rare case of cyclin D1-positive diffuse large B-cell lymphoma in the right tonsil of a 50-year-old man. Computed tomographic imaging detected a mass, about 2.5 cm × 1.8 cm in size, in the left side of the oropharynx. DIAGNOSES: Microscopically, the tumor cells were located under the pharyngeal mucosa and diffusely arranged. The tumor cells were large, with marked nuclear atypia. On performing immunohistochemistry, the tumor cells showed diffuse positive staining for CD10, CD20, cyclin D1, and Pax-5, and negative staining for CD3, CD15, CD30, CD56, and CK. Bcl-6 and Mum-1 expression were observed in 60% and 80% of tumor cells, respectively. The tumor Ki67 index was about 60%. Based on these findings, The tumor was diagnosed as a rare cyclin D1-positive diffuse large B-cell lymphoma rather than a mantle cell lymphoma. CONCLUSION: Cyclin D1-positive large B-cell lymphoma is rare, but as large B-cell lymphoma is a common type of lymphoma, cyclin D1-positive large B-cell lymphoma should be considered a major possibility during differential diagnosis, including in the tonsils.
[Mh] Termos MeSH primário: Linfoma Difuso de Grandes Células B/patologia
Tonsila Palatina/patologia
[Mh] Termos MeSH secundário: Quimiorradioterapia
Ciclina D1/imunologia
Centro Germinativo
Seres Humanos
Linfoma Difuso de Grandes Células B/diagnóstico por imagem
Linfoma Difuso de Grandes Células B/terapia
Masculino
Meia-Idade
Fator de Transcrição PAX5/imunologia
Tonsila Palatina/diagnóstico por imagem
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (PAX5 Transcription Factor); 0 (PAX5 protein, human); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006311



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