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[PMID]:29318382
[Au] Autor:Mazzoccoli L; Robaina MC; Apa AG; Bonamino M; Pinto LW; Queiroga E; Bacchi CE; Klumb CE
[Ad] Endereço:Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer, Rio de Janeiro, Brazil.
[Ti] Título:MiR-29 silencing modulates the expression of target genes related to proliferation, apoptosis and methylation in Burkitt lymphoma cells.
[So] Source:J Cancer Res Clin Oncol;144(3):483-497, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Burkitt lymphoma (BL) is a B-cell lymphoma frequently diagnosed in children. It is characterized by MYC translocations, which lead to the constitutive expression of the MYC oncogene. MYC contributes to miR-29 repression through an E-box MYC binding site on the miR-29b-1/miR-29a promoter region. We evaluated the role of miR-29a/b/c and their predicted targets in BL pathogenesis. METHODS: Mature sequences of miR-29a/b/c were transfected to the BL cell lines BL41 and Raji, and evaluated for DNMT3B, MCL1, BIM, CDK6, AKT and TCL1 protein expression as well as for MCL-1 and CDK6 mRNA expression. BL cells were treated with 5-aza-2'-deoxycytidine (decitabine) and evaluated for miR29 expressions and methylation status. DNMT3B inhibition was performed by DNMT3B siRNA. RESULTS: Ectopic expression of miR-29s in BL cells decreased CDK6, DNMT3B, TCL1 and MCL-1 protein levels, but CDK6 and MCL-1 mRNA expression was unaffected by miR-29. Decitabine enhanced miR-29 expression levels and decreased CDK6 protein expression. Additionally, inhibition of DNMT3B by siRNA increased miR-29a/b expression. Notably, the miR-29a/b1 and miR-29b2/c promoter genes showed methylated CpG sequences that were demethylated after decitabine treatments. Furthermore, MYC-negative tumours had higher levels of miR-29 expression compared with MYC-translocated cases, suggesting that MYC regulates miR-29 in BL tumours. CONCLUSIONS: Our results suggest a significant role for miR-29s in BL pathogenesis in altering the expression of targets involved in critical cancer pathways, such as cell cycle control, apoptosis inhibition and DNA methylation. Moreover, methylation-mediated miR-29 epigenetic silencing may occur during BL development.
[Mh] Termos MeSH primário: Apoptose/genética
Linfoma de Burkitt/genética
Proliferação Celular/genética
Metilação de DNA/genética
MicroRNAs/genética
[Mh] Termos MeSH secundário: Adolescente
Linfoma de Burkitt/patologia
Linhagem Celular Tumoral
Criança
Pré-Escolar
Epigênese Genética
Regulação Neoplásica da Expressão Gênica
Inativação Gênica/fisiologia
Seres Humanos
Lactente
Recém-Nascido
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN29 microRNA, human); 0 (MicroRNAs)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2575-3


  2 / 9748 MEDLINE  
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[PMID]:28465297
[Au] Autor:Kaymaz Y; Oduor CI; Yu H; Otieno JA; Ong'echa JM; Moormann AM; Bailey JA
[Ad] Endereço:Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, Massachusetts.
[Ti] Título:Comprehensive Transcriptome and Mutational Profiling of Endemic Burkitt Lymphoma Reveals EBV Type-Specific Differences.
[So] Source:Mol Cancer Res;15(5):563-576, 2017 05.
[Is] ISSN:1557-3125
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endemic Burkitt lymphoma (eBL) is the most common pediatric cancer in malaria-endemic equatorial Africa and nearly always contains Epstein-Barr virus (EBV), unlike sporadic Burkitt lymphoma (sBL) that occurs with a lower incidence in developed countries. Given these differences and the variable clinical presentation and outcomes, we sought to further understand pathogenesis by investigating transcriptomes using RNA sequencing (RNAseq) from multiple primary eBL tumors compared with sBL tumors. Within eBL tumors, minimal expression differences were found based on: anatomical presentation site, in-hospital survival rates, and EBV genome type, suggesting that eBL tumors are homogeneous without marked subtypes. The outstanding difference detected using surrogate variable analysis was the significantly decreased expression of key genes in the immunoproteasome complex ( /ß1i, /ß2i, /ß5i, and /PA28ß) in eBL tumors carrying type 2 EBV compared with type 1 EBV. Second, in comparison with previously published pediatric sBL specimens, the majority of the expression and pathway differences was related to the PTEN/PI3K/mTOR signaling pathway and was correlated most strongly with EBV status rather than geographic designation. Third, common mutations were observed significantly less frequently in eBL tumors harboring EBV type 1, with mutation frequencies similar between tumors with EBV type 2 and without EBV. In addition to the previously reported genes, a set of new genes mutated in BL, including , and were identified. Overall, these data establish that EBV, particularly EBV type 1, supports BL oncogenesis, alleviating the need for certain driver mutations in the human genome. IMPLICATIONS: Genomic and mutational analyses of Burkitt lymphoma tumors identify key differences based on viral content and clinical outcomes suggesting new avenues for the development of prognostic molecular biomarkers and therapeutic interventions.
[Mh] Termos MeSH primário: Linfoma de Burkitt/genética
Infecções por Vírus Epstein-Barr/genética
Perfilação da Expressão Gênica/métodos
Herpesvirus Humano 4/classificação
Mutação
[Mh] Termos MeSH secundário: Adolescente
Linfoma de Burkitt/virologia
Criança
Pré-Escolar
Doenças Endêmicas
Feminino
Redes Reguladoras de Genes
Genoma Viral
Herpesvirus Humano 4/genética
Seres Humanos
Quênia/epidemiologia
Masculino
Taxa de Mutação
Análise de Sequência de RNA
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1158/1541-7786.MCR-16-0305


  3 / 9748 MEDLINE  
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[PMID]:28748558
[Au] Autor:Ott G
[Ad] Endereço:Department of Clinical Pathology, Robert-Bosch-Krankenhaus, Stuttgart, Germany.
[Ti] Título:Aggressive B-cell lymphomas in the update of the 4th edition of the World Health Organization classification of haematopoietic and lymphatic tissues: refinements of the classification, new entities and genetic findings.
[So] Source:Br J Haematol;178(6):871-887, 2017 09.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The update of the 4th edition of the World Health Organization Classification of Haematopoietic and Lymphatic Tissues portends important new findings and concepts in the diagnosis, classification and biology of lymphomas. This review summarizes the basic concepts and cornerstones of the classification of aggressive B-cell lymphomas and details the major changes. Of importance, there is a new concept of High-grade B-cell lymphomas (HGBL), partly replacing the provisional entity of B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma, the so-called grey zone lymphomas. They either harbour MYC translocations together with a BCL2 and/or a BCL6 rearrangement (HGBL-Double Hit) or HGBL, not otherwise specified (NOS), lacking a double or triple hit constellation. In addition, the requirement for providing the cell-of-origin classification in the diagnostic work-up of DLBCLs, the role of MYC alterations in DLBCL subtypes, and newer findings in the specific variants/subtypes are highlighted.
[Mh] Termos MeSH primário: Linfoma de Células B/classificação
[Mh] Termos MeSH secundário: Linfoma de Burkitt/classificação
Linfoma de Burkitt/genética
Linfoma de Burkitt/patologia
Genes myc/genética
Seres Humanos
Linfoma de Células B/genética
Linfoma de Células B/patologia
Linfoma Difuso de Grandes Células B/classificação
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/patologia
Mutação
Gradação de Tumores
Organização Mundial da Saúde
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14744


  4 / 9748 MEDLINE  
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[PMID]:29209924
[Au] Autor:Oosten LEM; Chamuleau MED; Thielen FW; de Wreede LC; Siemes C; Doorduijn JK; Smeekes OS; Kersten MJ; Hardi L; Baars JW; Demandt AMP; Stevens WBC; Nijland M; van Imhoff GW; Brouwer R; Uyl-de Groot CA; Kluin PM; de Jong D; Veelken H
[Ad] Endereço:Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands. l.e.m.oosten@lumc.nl.
[Ti] Título:Treatment of sporadic Burkitt lymphoma in adults, a retrospective comparison of four treatment regimens.
[So] Source:Ann Hematol;97(2):255-266, 2018 Feb.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Burkitt lymphoma is an aggressive B cell malignancy accounting for 1-2% of all adult lymphomas. Treatment with dose-intensive, multi-agent chemotherapy is effective but associated with considerable toxicity. In this observational study, we compared real-world efficacy, toxicity, and costs of four frequently employed treatment strategies for Burkitt lymphoma: the Lymphome Malins B (LMB), the Berlin-Frankfurt-Münster (BFM), the HOVON, and the CODOX-M/IVAC regimens. We collected data from 147 adult patients treated in eight referral centers. Following central pathology assessment, 105 of these cases were accepted as Burkitt lymphoma, resulting in the following treatment groups: LMB 36 patients, BFM 19 patients, HOVON 29 patients, and CODOX-M/IVAC 21 patients (median age 39 years, range 14-74; mean duration of follow-up 47 months). There was no significant difference between age, sex ratio, disease stage, or percentage HIV-positive patients between the treatment groups. Five-year progression-free survival (69%, p = 0.966) and 5-year overall survival (69%, p = 0.981) were comparable for all treatment groups. Treatment-related toxicity was also comparable with only hepatotoxicity seen more frequently in the CODOX/M-IVAC group (p = 0.004). Costs were determined by the number of rituximab gifts and the number of inpatients days. Overall, CODOX-M/IVAC had the most beneficial profile with regards to costs, treatment duration, and percentage of patients completing planned treatment. We conclude that the four treatment protocols for Burkitt lymphoma yield nearly identical results with regards to efficacy and safety but differ in treatment duration and costs. These differences may help guide future choice of treatment.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linfoma de Burkitt/tratamento farmacológico
Análise Custo-Benefício
Infecções por HIV/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Linfoma de Burkitt/complicações
Linfoma de Burkitt/economia
Linfoma de Burkitt/mortalidade
Carmustina/economia
Carmustina/uso terapêutico
Ciclofosfamida/economia
Ciclofosfamida/uso terapêutico
Citarabina/economia
Citarabina/uso terapêutico
Etoposídeo/economia
Etoposídeo/uso terapêutico
Feminino
Infecções por HIV/complicações
Infecções por HIV/economia
Infecções por HIV/mortalidade
Seres Humanos
Ifosfamida/economia
Ifosfamida/uso terapêutico
Masculino
Melfalan/economia
Melfalan/uso terapêutico
Metotrexato/economia
Metotrexato/uso terapêutico
Meia-Idade
Estadiamento de Neoplasias
Estudos Retrospectivos
Rituximab/economia
Rituximab/uso terapêutico
Análise de Sobrevida
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Nm] Nome de substância:
04079A1RDZ (Cytarabine); 4F4X42SYQ6 (Rituximab); 6PLQ3CP4P3 (Etoposide); 8N3DW7272P (Cyclophosphamide); Q41OR9510P (Melphalan); U68WG3173Y (Carmustine); UM20QQM95Y (Ifosfamide); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3167-7


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[PMID]:29245266
[Au] Autor:Gurzu S; Bara T; Bara TJ; Turcu M; Mardare CV; Jung I
[Ad] Endereço:aDepartment of PathologybDepartment of Pathology, Clinical County Emergency HospitalcDepartment of Surgery, University of Medicine and Pharmacy, Tirgu-Mures, Romania.
[Ti] Título:Gastric Burkitt lymphoma: A case report and literature review.
[So] Source:Medicine (Baltimore);96(49):e8954, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Burkitt lymphoma (BL) is an endemic tumor in Africa but rare sporadic cases are diagnosed in Europe. PATIENT CONCERNS: A 60-year-old woman was hospitalized with fulminant hematemesis and a history of recurring melena. DIAGNOSES: The upper gastrointestinal endoscopy revealed a tumor of the antrum. INTERVENTIONS: Emergency gastrectomy was performed. OUTCOMES: Gross findings revealed an ulcerated tumor with elevated margins and several perigastric and extragastric lymph nodes. Histological examination showed proliferation of atypical lymphocytes with a Ki67 index of 100%; they were marked by CD20, CD79a, bcl-6, and CD10 and were negative for CD3, CD5, CD23, TdT, bcl-2, and Cyclin D1. The tumor cells crossed the serosa and presented invasion of the lymph nodes. The patient died 10 days after surgery due to bronchopneumonia and acute renal failure. LESSONS: In our department, only one gastric BL was diagnosed in a 61 consecutive lymphomas of the gastrointestinal tract (1.64%). Less than 200 reports about gastric-BL have been published to date. This case highlights the difficulty of diagnosis of rare variants of aggressive gastric lymphomas in medium-income countries without screening programmes.
[Mh] Termos MeSH primário: Linfoma de Burkitt/diagnóstico
Linfoma de Burkitt/cirurgia
Neoplasias Gástricas/diagnóstico
Neoplasias Gástricas/cirurgia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/análise
Linfoma de Burkitt/patologia
Emergências
Evolução Fatal
Feminino
Gastrectomia
Gastroscopia
Seres Humanos
Metástase Linfática
Meia-Idade
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171225
[Lr] Data última revisão:
171225
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008954


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[PMID]:28973700
[Au] Autor:Alsadi A; Lin D; Alnajar H; Brickman A; Martyn C; Gattuso P
[Ad] Endereço:From the Department of Pathology, Rush University Medical Center, Chicago, Illinois.
[Ti] Título:Hematologic Malignancies Discovered on Investigation of Breast Abnormalities.
[So] Source:South Med J;110(10):614-620, 2017 Oct.
[Is] ISSN:1541-8243
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Hematological malignancies of the breast share a presentation similar to primary breast carcinomas but differ substantially in therapeutic approach and clinical outcomes. In this study, we investigate the frequency of hematological malignancies, their relative primary and secondary occurrences, and further characterize the distinct histopathologies of these malignancies with a special focus on lymphomas. To our knowledge this is one of the largest and most comprehensive studies of breast hematologic malignancies. METHODS: We conducted a retrospective review of our institution's pathology database for hematologic neoplasms diagnosed in breast tissue during a period of 22 years (1992-2014). Clinical characteristics, patient history, histologic subtype, and patient outcomes were analyzed. RESULTS: We identified 52 cases; 46 lymphomas, 4 plasmacytomas, and 2 myeloid sarcomas. The lymphoma cases were 15 diffuse large B-cell lymphomas (DLBCLs), 14 follicular lymphomas (FLs), 8 marginal zone lymphomas (MZLs), 2 anaplastic large T-cell lymphomas, 2 peripheral T-cell lymphomas-not otherwise specified, 1 each of small lymphocytic lymphoma, Burkitt lymphoma, mantle cell lymphoma, B-cell lymphoblastic lymphoma, and T-cell lymphoblastic lymphoma. In total, 30 cases were primary and 22 cases were secondary to the breast. Primary lymphomas accounted for 60% of lymphomas. Most FLs and almost all MZLs were primary. CONCLUSIONS: Primary hematological malignancies of the breast are more common than secondary: 58 % versus 42%. This finding is more evident in lymphomas: 63% versus 37%. The most common hematological malignancy in our study was DLBCL, followed by FL and MZL. Most FLs and almost all MZLs were primary. At the same time, the percentage of primary DLBCLs in our study is lower than the percentage reported in previous studies. We suggest that this could be the result of transformation from low-grade lymphomas. Although rare, hematological malignancies of the breast warrant a higher level of clinical suspicion as they present similarly to breast carcinomas but require a substantially different therapeutic approach.
[Mh] Termos MeSH primário: Neoplasias da Mama/diagnóstico
Carcinoma/diagnóstico
Neoplasias Hematológicas/diagnóstico
Linfoma/diagnóstico
Plasmocitoma/diagnóstico
Sarcoma Mieloide/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Neoplasias da Mama/patologia
Neoplasias da Mama/secundário
Linfoma de Burkitt/diagnóstico
Linfoma de Burkitt/patologia
Diagnóstico Diferencial
Feminino
Neoplasias Hematológicas/patologia
Seres Humanos
Leucemia Linfocítica Crônica de Células B/diagnóstico
Leucemia Linfocítica Crônica de Células B/patologia
Linfoma/patologia
Linfoma de Zona Marginal Tipo Células B/diagnóstico
Linfoma de Zona Marginal Tipo Células B/patologia
Linfoma Folicular/diagnóstico
Linfoma Folicular/patologia
Linfoma Difuso de Grandes Células B/diagnóstico
Linfoma Difuso de Grandes Células B/patologia
Linfoma Anaplásico de Células Grandes/diagnóstico
Linfoma Anaplásico de Células Grandes/patologia
Linfoma de Célula do Manto/diagnóstico
Linfoma de Célula do Manto/patologia
Linfoma de Células T/diagnóstico
Linfoma de Células T/patologia
Meia-Idade
Plasmocitoma/patologia
Leucemia-Linfoma Linfoblástico de Células Precursoras B/diagnóstico
Leucemia-Linfoma Linfoblástico de Células Precursoras B/patologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/diagnóstico
Leucemia-Linfoma Linfoblástico de Células T Precursoras/patologia
Estudos Retrospectivos
Sarcoma Mieloide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.14423/SMJ.0000000000000710


  7 / 9748 MEDLINE  
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[PMID]:28902524
[Au] Autor:Guja K; Liehr T; Rincic M; Kosyakova N; Hussein Azawi SS
[Ad] Endereço:Institute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany.
[Ti] Título:Molecular Cytogenetic Characterization Identified the Murine B-Cell Lymphoma Cell Line A-20 as a Model for Sporadic Burkitt's Lymphoma.
[So] Source:J Histochem Cytochem;65(11):669-677, 2017 Nov.
[Is] ISSN:1551-5044
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Here, we report the first molecular cytogenetic characterization of the BALB/cAnN mouse derived B-cell non-Hodgkin lymphoma (B-cell NHL) cell lines A-20. Even though previously used as a model for testing of, for example, dexametason, up to present, no data in the genetic properties of A-20 were available. The present study closed this gap and provides evidence that A-20 is a model for B-cell NHL subgroup sporadic Burkitt's lymphoma. C-myc oncogene is involved in a translocation and copy number alterations as gain of murine 14q material could be observed. Interestingly, the cell line showed the karyotype 39,X,-X or -Y,t(2;15)(qE5;qD2),del(6)(qB3qC3),del(9)(qA3qA4),dup(14)(qE1qE4) in ~95% of the cells, being exceptionally stable for cell lines being established 38 years ago. Still, ~5% of the cells showed polyploidization followed by chromothripsis. It remains to be determined if this can be observed also in other cell lines, just has not been reported yet, and/or if it is a unique feature of A-20. Overall, finally here, the necessary genetic data to identify A-20 as a model for human sporadic Burkitt's lymphoma are provided.
[Mh] Termos MeSH primário: Linfoma de Burkitt/genética
Modelos Animais de Doenças
Linfoma de Células B/genética
[Mh] Termos MeSH secundário: Animais
Linfoma de Burkitt/patologia
Linhagem Celular Tumoral
Citogenética
Hibridização in Situ Fluorescente
Cariotipagem
Linfoma de Células B/patologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1369/0022155417731319


  8 / 9748 MEDLINE  
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[PMID]:28807996
[Au] Autor:Bertocci B; Lecoeuche D; Sterlin D; Kühn J; Gaillard B; De Smet A; Lembo F; Bole-Feysot C; Cagnard N; Fadeev T; Dahan A; Weill JC; Reynaud CA
[Ad] Endereço:Équipe Développement du Systéme Immunitaire, Institut Necker-Enfant Malades, INSERM U1151-CNRS UMR8253, Faculté de Médecine Paris Decartes, Université Paris Descartes, Sorbone Paris Cité, 75993 Paris Cedex 14, France; barbara.bertocci@inserm.fr.
[Ti] Título:Klhl6 Deficiency Impairs Transitional B Cell Survival and Differentiation.
[So] Source:J Immunol;199(7):2408-2420, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Klhl6 belongs to the KLHL gene family, which is composed of an N-terminal BTB-POZ domain and four to six Kelch motifs in tandem. Several of these proteins function as adaptors of the Cullin3 E3 ubiquitin ligase complex. In this article, we report that Klhl6 deficiency induces, as previously described, a 2-fold reduction in mature B cells. However, we find that this deficit is centered on the inability of transitional type 1 B cells to survive and to progress toward the transitional type 2 B cell stage, whereas cells that have passed this step generate normal germinal centers (GCs) upon a T-dependent immune challenge. Klhl6-deficient type 1 B cells showed a 2-fold overexpression of genes linked with cell proliferation, including most targets of the anaphase-promoting complex/cyclosome complex, a set of genes whose expression is precisely downmodulated upon culture of splenic transitional B cells in the presence of BAFF. These results thus suggest a delay in the differentiation process of Klhl6-deficient B cells between the immature and transitional stage. We further show, in the BL2 Burkitt's lymphoma cell line, that KLHL6 interacts with Cullin3, but also that it binds to HBXIP/Lamtor5, a protein involved in cell-cycle regulation and cytokinesis. Finally, we report that KLHL6, which is recurrently mutated in B cell lymphomas, is an off-target of the normal somatic hypermutation process taking place in GC B cells in both mice and humans, thus leaving open whether, despite the lack of impact of Klhl6 deficiency on GC B cell expansion, mutants could contribute to the oncogenic process.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Proteínas de Transporte/fisiologia
Centro Germinativo/citologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Linfoma de Burkitt/patologia
Proteínas de Transporte/genética
Diferenciação Celular
Linhagem Celular
Proliferação Celular
Centro Germinativo/imunologia
Seres Humanos
Linfoma de Células B/genética
Linfoma de Células B/patologia
Camundongos
Mutação
Células Precursoras de Linfócitos B/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (KLHL6 protein, human); 0 (Klhl6 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700708


  9 / 9748 MEDLINE  
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[PMID]:28801451
[Au] Autor:Bouska A; Bi C; Lone W; Zhang W; Kedwaii A; Heavican T; Lachel CM; Yu J; Ferro R; Eldorghamy N; Greiner TC; Vose J; Weisenburger DD; Gascoyne RD; Rosenwald A; Ott G; Campo E; Rimsza LM; Jaffe ES; Braziel RM; Siebert R; Miles RR; Dave S; Reddy A; Delabie J; Staudt LM; Song JY; McKeithan TW; Fu K; Green M; Chan WC; Iqbal J
[Ad] Endereço:Pathology and Microbiology and.
[Ti] Título:Adult high-grade B-cell lymphoma with Burkitt lymphoma signature: genomic features and potential therapeutic targets.
[So] Source:Blood;130(16):1819-1831, 2017 Oct 19.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The adult high-grade B-cell lymphomas sharing molecular features with Burkitt lymphoma (BL) are highly aggressive lymphomas with poor clinical outcome. High-resolution structural and functional genomic analysis of adult Burkitt lymphoma (BL) and high-grade B-cell lymphoma with BL gene signature (adult-molecularly defined BL [mBL]) revealed the MYC-ARF-p53 axis as the primary deregulated pathway. Adult-mBL had either unique or more frequent genomic aberrations (del13q14, del17p, gain8q24, and gain18q21) compared with pediatric-mBL, but shared commonly mutated genes. Mutations in genes promoting the tonic B-cell receptor (BCR)→PI3K pathway ( and ) did not differ by age, whereas effectors of chronic BCR→NF-κB signaling were associated with adult-mBL. A subset of adult-mBL had translocation and mutation and elevated mRNA and protein expression, but had a mutation profile similar to mBL. These double-hit lymphomas may have arisen from a tumor precursor that acquired both and translocations and/or ( ) mutation. Gain/amplification of and its paralogue loci was observed in 50% of adult-mBL. In vitro studies suggested 's role in constitutive activation of BCR signaling and sensitivity to ibrutinib. Overall integrative analysis identified an interrelated gene network affected by copy number and mutation, leading to disruption of the p53 pathway and the BCR→PI3K or NF-κB activation, which can be further exploited in vivo by small-molecule inhibitors for effective therapy in adult-mBL.
[Mh] Termos MeSH primário: Linfoma de Burkitt/genética
Regulação Neoplásica da Expressão Gênica
Linfoma de Células B/genética
Transcriptoma
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Linfócitos B/patologia
Linhagem Celular Tumoral
Criança
Pré-Escolar
Feminino
Seres Humanos
Imunofenotipagem
Linfoma de Células B/patologia
Masculino
Meia-Idade
Terapia de Alvo Molecular
Gradação de Tumores
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-02-767335


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[PMID]:28707393
[Au] Autor:Mawson AR; Majumdar S
[Ad] Endereço:Professor, Department of Epidemiology and Biostatistics, School of Public Health, Jackson State University, Jackson, MS.
[Ti] Título:Malaria, Epstein-Barr virus infection and the pathogenesis of Burkitt's lymphoma.
[So] Source:Int J Cancer;141(9):1849-1855, 2017 Nov 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A geographical and causal connection has long been recognized between malaria, Epstein-Barr virus (EBV) infection and Burkitt's lymphoma (BL), but the underlying mechanisms remain obscure. Potential clues are that the malaria parasite Plasmodium falciparum selectively absorbs vitamin A from the host and depends on it for its biological activities; secondly, alterations in vitamin A (retinoid) metabolism have been implicated in many forms of cancer, including BL. The first author has proposed that the merozoite-stage malaria parasite, emerging from the liver, uses its absorbed vitamin A as a cell membrane destabilizer to invade the red blood cells, causing anemia and other signs and symptoms of the disease as manifestations of an endogenous form of hypervitaminosis A (Mawson AR, Path Global Health 2013;107(3):122-9). Repeated episodes of malaria would therefore be expected to expose the tissues of affected individuals to potentially toxic doses of vitamin A. It is proposed that such episodes activate latent EBV infection, which in turn activates retinoid-responsive genes. Expression of these genes enhances viral replication and induces germinal center (GC) B cell expansion, activation-induced cytidine deaminase (AID) expression, and c-myc translocation, which in turn predisposes to BL. Thus, an endogenous form of retinoid toxicity related to malaria infection may be the common factor linking frequent malaria, EBV infection and BL, whereby prolonged exposure of lymphatic tissues to high concentrations of retinoids may combine to induce B-cell translocation and increase the risk of Burkitt's lymphoma.
[Mh] Termos MeSH primário: Linfoma de Burkitt/parasitologia
Linfoma de Burkitt/virologia
Infecções por Vírus Epstein-Barr/metabolismo
Malária Falciparum/metabolismo
[Mh] Termos MeSH secundário: Linfócitos B/metabolismo
Linfócitos B/parasitologia
Linfócitos B/patologia
Linfócitos B/virologia
Linfoma de Burkitt/complicações
Linfoma de Burkitt/metabolismo
Infecções por Vírus Epstein-Barr/complicações
Infecções por Vírus Epstein-Barr/virologia
Herpesvirus Humano 4/patogenicidade
Seres Humanos
Malária Falciparum/complicações
Malária Falciparum/parasitologia
Malária Falciparum/virologia
Plasmodium falciparum/patogenicidade
Vitamina A/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
11103-57-4 (Vitamin A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30885



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