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[PMID]:28724766
[Au] Autor:Ishihara Y; Tanaka Y; Kobayashi S; Kawamura K; Nakasone H; Gomyo A; Hayakawa J; Tamaki M; Akahoshi Y; Harada N; Kusuda M; Kameda K; Ugai T; Wada H; Sakamoto K; Sato M; Terasako-Saito K; Kikuchi M; Kimura SI; Tanihara A; Kako S; Uchimaru K; Kanda Y
[Ad] Endereço:Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan.
[Ti] Título:A Unique T-Cell Receptor Amino Acid Sequence Selected by Human T-Cell Lymphotropic Virus Type 1 Tax -Specific Cytotoxic T Cells in HLA-A24:02-Positive Asymptomatic Carriers and Adult T-Cell Leukemia/Lymphoma Patients.
[So] Source:J Virol;91(19), 2017 Oct 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that the T-cell receptor (TCR) repertoire of human T-cell lymphotropic virus type 1 (HTLV-1) Tax -specific CD8 cytotoxic T cells (Tax -CTLs) was highly restricted and a particular amino acid sequence motif, the PDR motif, was conserved among HLA-A*24:02-positive (HLA-A*24:02 ) adult T-cell leukemia/lymphoma (ATL) patients who had undergone allogeneic hematopoietic cell transplantation (allo-HSCT). Furthermore, we found that donor-derived PDR CTLs selectively expanded in ATL long-term HSCT survivors with strong CTL activity against HTLV-1. On the other hand, the TCR repertoires in Tax -CTLs of asymptomatic HTLV-1 carriers (ACs) remain unclear. In this study, we directly identified the DNA sequence of complementarity-determining region 3 (CDR3) of the TCR-ß chain of Tax -CTLs at the single-cell level and compared not only the TCR repertoires but also the frequencies and phenotypes of Tax -CTLs between ACs and ATL patients. We did not observe any essential difference in the frequencies of Tax -CTLs between ACs and ATL patients. In the single-cell TCR repertoire analysis of Tax -CTLs, 1,458 Tax -CTLs and 140 clones were identified in this cohort. Tax -CTLs showed highly restricted TCR repertoires with a strongly biased usage of BV7, and PDR, the unique motif in TCR-ß CDR3, was exclusively observed in all ACs and ATL patients. However, there was no correlation between PDR CTL frequencies and HTLV-1 proviral load (PVL). In conclusion, we have identified, for the first time, a unique amino acid sequence, PDR, as a public TCR-CDR3 motif against Tax in HLA-A*24:02 HTLV-1-infected individuals. Further investigations are warranted to elucidate the role of the PDR CTL response in the progression from carrier state to ATL. ATL is an aggressive T-cell malignancy caused by HTLV-1 infection. The HTLV-1 regulatory protein Tax aggressively promotes the proliferation of HTLV-1-infected lymphocytes and is also a major target antigen for CD8 CTLs. In our previous evaluation of Tax -CTLs, we found that a unique amino acid sequence motif, PDR, in CDR3 of the TCR-ß chain of Tax -CTLs was conserved among ATL patients after allo-HSCT. Furthermore, the PDR Tax -CTL clones selectively expanded and showed strong cytotoxic activities against HTLV-1. On the other hand, it remains unclear how Tax -CTL repertoire exists in ACs. In this study, we comprehensively compared Tax-specific TCR repertoires at the single-cell level between ACs and ATL patients. Tax -CTLs showed highly restricted TCR repertoires with a strongly biased usage of BV7, and PDR, the unique motif in TCR-ß CDR3, was conserved in all ACs and ATL patients, regardless of clinical subtype in HTLV-1 infection.
[Mh] Termos MeSH primário: Produtos do Gene tax/imunologia
Antígeno HLA-A24/imunologia
Vírus 1 Linfotrópico T Humano/imunologia
Leucemia-Linfoma de Células T do Adulto/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Linfócitos T Citotóxicos/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos/genética
Antígenos CD7/metabolismo
Molécula 1 de Adesão Celular
Moléculas de Adesão Celular/metabolismo
Células Cultivadas
Produtos do Gene tax/genética
Antígeno HLA-A24/genética
Infecções por HTLV-I/patologia
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
Imunoglobulinas/metabolismo
Memória Imunológica/imunologia
Leucemia-Linfoma de Células T do Adulto/genética
Receptores de Antígenos de Linfócitos T/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (CADM1 protein, human); 0 (Cell Adhesion Molecule-1); 0 (Cell Adhesion Molecules); 0 (Gene Products, tax); 0 (HLA-A24 Antigen); 0 (Immunoglobulins); 0 (Receptors, Antigen, T-Cell); 0 (tax protein, Human T-lymphotrophic virus 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE


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[PMID]:28539325
[Au] Autor:Gomes-Silva D; Srinivasan M; Sharma S; Lee CM; Wagner DL; Davis TH; Rouce RH; Bao G; Brenner MK; Mamonkin M
[Ad] Endereço:Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, TX.
[Ti] Título:CD7-edited T cells expressing a CD7-specific CAR for the therapy of T-cell malignancies.
[So] Source:Blood;130(3):285-296, 2017 Jul 20.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extending the success of chimeric antigen receptor (CAR) T cells to T-cell malignancies is problematic because most target antigens are shared between normal and malignant cells, leading to CAR T-cell fratricide. CD7 is a transmembrane protein highly expressed in acute T-cell leukemia (T-ALL) and in a subset of peripheral T-cell lymphomas. Normal expression of CD7 is largely confined to T cells and natural killer (NK) cells, reducing the risk of off-target-organ toxicity. Here, we show that the expression of a CD7-specific CAR impaired expansion of transduced T cells because of residual CD7 expression and the ensuing fratricide. We demonstrate that targeted genomic disruption of the CD7 gene prevented this fratricide and enabled expansion of CD7 CAR T cells without compromising their cytotoxic function. CD7 CAR T cells produced robust cytotoxicity against malignant T-cell lines and primary tumors and were protective in a mouse xenograft model of T-ALL. Although CD7 CAR T cells were also toxic against unedited (CD7 ) T and NK lymphocytes, we show that the CD7-edited T cells themselves can respond to viral peptides and therefore could be protective against pathogens. Hence, genomic disruption of a target antigen overcomes fratricide of CAR T cells and establishes the feasibility of using CD7 CAR T cells for the targeted therapy of T-cell malignancies.
[Mh] Termos MeSH primário: Antígenos CD7/imunologia
Citotoxicidade Imunológica
Imunoterapia Adotiva/métodos
Leucemia-Linfoma Linfoblástico de Células T Precursoras/terapia
Receptores de Antígenos de Linfócitos T/genética
Proteínas Recombinantes de Fusão/imunologia
Linfócitos T/transplante
[Mh] Termos MeSH secundário: Animais
Antígenos CD7/genética
Linhagem Celular Tumoral
Proliferação Celular
Feminino
Expressão Gênica
Inativação Gênica
Seres Humanos
Células Matadoras Naturais/citologia
Células Matadoras Naturais/imunologia
Ativação Linfocitária
Masculino
Camundongos
Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética
Leucemia-Linfoma Linfoblástico de Células T Precursoras/imunologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/patologia
Receptores de Antígenos de Linfócitos T/imunologia
Proteínas Recombinantes de Fusão/genética
Linfócitos T/citologia
Linfócitos T/imunologia
Transdução Genética
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (Receptors, Antigen, T-Cell); 0 (Recombinant Fusion Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-01-761320


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[PMID]:27788919
[Au] Autor:Iliadis A; Koletsa T; Kostopoulos I
[Ad] Endereço:Department of Pathology, Faculty of Medicine, Aristotle University, Thessaloniki, Greece.
[Ti] Título:Aberrant expression of T-cell marker CD7 in HIV negative intestinal plasmablastic lymphoma.
[So] Source:Pathology;48(7):731-733, 2016 Dec.
[Is] ISSN:1465-3931
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Antígenos CD7/biossíntese
Neoplasias Intestinais/patologia
Linfoma Plasmablástico/patologia
[Mh] Termos MeSH secundário: Idoso
Biomarcadores Tumorais/análise
Infecções por HIV
Seres Humanos
Imuno-Histoquímica
Imunofenotipagem
Neoplasias Intestinais/imunologia
Masculino
Linfoma Plasmablástico/imunologia
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (Biomarkers, Tumor)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


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[PMID]:27348401
[Au] Autor:Edwin C; Dean J; Bonnett L; Phillips K; Keenan R
[Ad] Endereço:Department of Women's and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
[Ti] Título:Non-tumour bone marrow lymphocytes correlate with improved overall survival in childhood acute lymphoblastic leukaemia.
[So] Source:Pediatr Blood Cancer;63(10):1848-51, 2016 Oct.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Composition of tumour immune cell infiltrates correlates with response to treatment and overall survival (OS) in several cancer settings. We retrospectively examined immune cells present in diagnostic bone marrow aspirates from paediatric patients with B-cell acute lymphoblastic leukaemia. Our analysis identified a sub-group (∼30% of patients) with >2.37% CD20 and >6.05% CD7 expression, which had 100% OS, and a sub-group (∼30% of patients) with ≤2.37% CD20 and ≤6.05% CD7 expression at increased risk of treatment failure (66.7% OS, P < 0.05). Immune cell infiltrate at diagnosis may predict treatment response and could provide a means to enhance immediate treatment risk stratification.
[Mh] Termos MeSH primário: Medula Óssea/patologia
Linfócitos/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras B/mortalidade
[Mh] Termos MeSH secundário: Antígenos CD20/análise
Antígenos CD7/análise
Criança
Pré-Escolar
Feminino
Seres Humanos
Masculino
Leucemia-Linfoma Linfoblástico de Células Precursoras B/imunologia
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD20); 0 (Antigens, CD7)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160628
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26093


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[PMID]:26242204
[Au] Autor:Fallah Azad V; Hedayati Asl AA; Tashvighi M; Niktoreh Mofrad N; Haghighi M; Mehrvar A
[Ad] Endereço:Research Department, Mahak's Pediatric Cancer Treatment and Research Center, Mahak Blvd., Oshan Blvd., Aghdasieh Ave, 1956993461, Tehran, Iran.
[Ti] Título:CD7 aberrant expression led to a lineage switch at relapsed childhood acute pre-B lymphoblastic leukemia.
[So] Source:Med Mol Morphol;49(1):53-6, 2016 Mar.
[Is] ISSN:1860-1499
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Immunophenotypic changes and lineage switch between diagnosis and relapse in acute lymphoblastic leukemia are uncommon and accompanied by poor outcomes. In this report, a 12-year-old boy with diagnosis of pre-B ALL with an aberrant expression of CD 7 is described. Patient was treated with the ALL-BFM 2000 protocol and suffered an episode of relapse with a lineage switch from pre-B ALL to T cell ALL. This report concludes that presence of aberrant expression of CD7 at diagnosis of pre-B ALL can have prognostic value of lineage switch to T cell ALL at relapse.
[Mh] Termos MeSH primário: Antígenos CD7/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras B/metabolismo
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Criança
Seres Humanos
Masculino
Leucemia-Linfoma Linfoblástico de Células Precursoras B/diagnóstico
Leucemia-Linfoma Linfoblástico de Células Precursoras B/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras B/patologia
Recidiva
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD7)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150806
[St] Status:MEDLINE
[do] DOI:10.1007/s00795-015-0117-0


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[PMID]:26104659
[Au] Autor:Oelschlaegel U; Alexander Röhnert M; Mohr B; Sockel K; Herold S; Ehninger G; Bornhäuser M; Thiede C; Platzbecker U
[Ad] Endereço:Medizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus, Dresden, Germany.
[Ti] Título:Clonal architecture of del(5q) myelodysplastic syndromes: aberrant CD5 or CD7 expression within the myeloid progenitor compartment defines a subset with high clonal burden.
[So] Source:Leukemia;30(2):517-20, 2016 Feb.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Antígenos CD7/análise
Antígenos CD5/análise
Deleção Cromossômica
Cromossomos Humanos Par 5
Síndromes Mielodisplásicas/genética
Células Progenitoras Mieloides/imunologia
[Mh] Termos MeSH secundário: Eritropoese
Citometria de Fluxo
Seres Humanos
Hibridização in Situ Fluorescente
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (CD5 Antigens)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150625
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2015.158


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[PMID]:26185316
[Au] Autor:Knez VM; Carstens BJ; Swisshelm KL; McGranahan AN; Liang X
[Ad] Endereço:From the Department of Pathology and.
[Ti] Título:Heterogeneity of Abnormal RUNX1 Leading to Clinicopathologic Variations in Childhood B-Lymphoblastic Leukemia.
[So] Source:Am J Clin Pathol;144(2):305-14, 2015 Aug.
[Is] ISSN:1943-7722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Abnormalities of the RUNX1 gene in childhood B-acute lymphoblastic leukemia (B-ALL) are manifested by ETV6-RUNX1 or RUNX1 amplification. A detailed comparison between the two regarding clinicopathologic features with genetic analysis has not been performed previously. This parallel study assessed how different RUNX1 abnormalities affect the clinicopathology of B-ALL. METHODS: We compared clinicopathologic factors, including age, sex, WBC count, cerebrospinal fluid (CSF) involvement, immunophenotype, and blast proliferation rate between B-ALL with RUNX1 amplification (10 cases) and B-ALL with ETV6-RUNX1 translocation (67 cases) in childhood B-ALL. RESULTS: CD7 was often expressed in RUNX1 amplification but not in ETV6-RUNX1 (44% vs 0%, P = .0001) and appeared to correlate with CSF involvement in the former group (3/4 [75%]). CD13 was often detected in ETV6-RUNX1 with additional RUNX1 gain (38%) with an even higher frequency in double ETV6-RUNX1 translocation (77%), but was not detected in RUNX1 amplification (0%, P < .05). Children with RUNX1 amplification were older and more often CSF positive, while those with ETV6-RUNX1 were younger, more frequently had hyperleukocytosis, and had higher blast proliferation rates. CONCLUSIONS: RUNX1 copy numbers seem to be proportional to the age of B-ALL onset and the frequency of CSF involvement, while RUNX1 amplification vs translocation causes aberrant expression of CD7 and CD13, respectively.
[Mh] Termos MeSH primário: Subunidade alfa 2 de Fator de Ligação ao Core/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
[Mh] Termos MeSH secundário: Adolescente
Idade de Início
Animais
Antígenos CD7/biossíntese
Antígenos CD7/imunologia
Antígenos CD13/biossíntese
Antígenos CD13/imunologia
Pré-Escolar
Feminino
Citometria de Fluxo
Amplificação de Genes
Seres Humanos
Imunofenotipagem
Hibridização in Situ Fluorescente
Masculino
Leucemia-Linfoma Linfoblástico de Células Precursoras/líquido cefalorraquidiano
Coelhos
Translocação Genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (Core Binding Factor Alpha 2 Subunit); 0 (RUNX1 protein, human); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150718
[St] Status:MEDLINE
[do] DOI:10.1309/AJCPVY5E5OMMYBFJ


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[PMID]:25703103
[Au] Autor:Kobayashi S; Watanabe E; Ishigaki T; Ohno N; Yuji K; Nakano K; Yamochi T; Watanabe N; Tojo A; Watanabe T; Uchimaru K
[Ad] Endereço:Division of Molecular Therapy, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
[Ti] Título:Advanced human T-cell leukemia virus type 1 carriers and early-stage indolent adult T-cell leukemia-lymphoma are indistinguishable based on CADM1 positivity in flow cytometry.
[So] Source:Cancer Sci;106(5):598-603, 2015 May.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We previously reported that the cell adhesion molecule 1 (CADM1) versus CD7 plot in flow cytometry reflects disease progression in human T-cell leukemia virus type 1 (HTLV-1) infection. In CD4(+) cells from peripheral blood, CADM1(-) CD7(+) (P), CADM1(+) CD7(dim) (D) and CADM1(+) CD7(-) (N) subpopulations are observed. The D and N subpopulations increase as asymptomatic HTLV-1 carriers (AC) progress to indolent adult T-cell leukemia-lymphoma (ATL) and the N subpopulation then expands in aggressive ATL. In the present study we examined whether the analysis can estimate the risk of developing ATL in advanced AC. Peripheral blood samples from AC (N = 41) and indolent ATL patients (N = 19) were analyzed by flow cytometry using the CADM1 versus CD7 plot for CD4(+) cells and inverse long PCR (clonality analysis) of FACS-sorted subpopulations. Almost all AC with a high HTLV-1 proviral load (>4 copies/100 cells) had a CADM1(+) (D + N) frequency of >10%. AC with 25% < CADM1(+) ≤ 50% contained expanded clones similar to smoldering-type ATL. In many patients in the 25% < CADM1(+) ≤ 50% group, the proportion of abnormal lymphocytes was distributed around the 5% line, which divides AC and smoldering-type ATL in Shimoyama's classification. In conclusion, the CADM1 versus CD7 plot is useful for selection of putative high-risk AC. The characteristics of some AC and smoldering ATL are said to be similar; however, long-term follow up is required and the clinical outcome (e.g. rate of transformation) of these cases should be used to determine whether to include them in the same clinical category.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/sangue
Citometria de Fluxo/métodos
Infecções por HTLV-I/patologia
Vírus 1 Linfotrópico T Humano/isolamento & purificação
Imunoglobulinas/sangue
Leucemia-Linfoma de Células T do Adulto/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD7/sangue
Molécula 1 de Adesão Celular
Feminino
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/patogenicidade
Seres Humanos
Leucemia-Linfoma de Células T do Adulto/diagnóstico
Leucemia-Linfoma de Células T do Adulto/virologia
Linfócitos/patologia
Linfócitos/virologia
Masculino
Meia-Idade
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (CADM1 protein, human); 0 (Cell Adhesion Molecule-1); 0 (Cell Adhesion Molecules); 0 (Immunoglobulins)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150224
[St] Status:MEDLINE
[do] DOI:10.1111/cas.12639


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[PMID]:25679063
[Au] Autor:Baqai J; Crisan D
[Ad] Endereço:Department of Clinical Pathology, William Beaumont Hospital, Beaumont Health System, MI.
[Ti] Título:Correlation of FLT3 mutations with expression of CD7 in acute myeloid leukemia.
[So] Source:Appl Immunohistochem Mol Morphol;23(2):104-8, 2015 Feb.
[Is] ISSN:1533-4058
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FLT3 mutations are common in acute myeloid leukemia (AML), particularly in cases with normal karyotype. Internal tandem duplication (ITD) and also point mutations affecting aspartic acid 835 (D835) are reported. A previous study demonstrated aberrant expression of CD7 on blasts in de novo AML cases with FLT3/ITD mutations. Our study goals are to expand the evaluation of this association to a larger group of patients; to evaluate the association of aberrant CD7 expression in AMLs with D835 mutation, not previously done; to evaluate if aberrant CD7 expression may serve as a surrogate marker for predicting FLT3 mutational status; to evaluate if combined FLT3 with NPM1 mutational status has a better correlation with CD7 expression. The FLT3 mutational analysis was performed on DNA extracted from 149 previously diagnosed AML cases with cytogenetics and flow cytometry evaluation available. Of 149 patients, 28 were positive for FLT3; CD7 was positive in 13 of 20 ITD-positive cases, 5 of 6 D835-positive cases, and 1 of 2 ITD/D835-positive cases. The association of CD7 positivity and FLT3 positivity was found to be significant. However, CD7 expression has a low positive predictive value of 30% and a negative predictive value of 90%. Because of the low positive predictive value, CD7 expression cannot be used as a surrogate marker for FLT3 positivity; even though the negative predictive value is higher, some cases that are FLT3 positive may be missed if CD7 expression would be used for screening.
[Mh] Termos MeSH primário: Antígenos CD7/metabolismo
Biomarcadores Tumorais/metabolismo
Leucemia Mieloide Aguda/diagnóstico
Mutação/genética
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Idoso
Análise Mutacional de DNA
Detecção Precoce de Câncer
Feminino
Regulação Leucêmica da Expressão Gênica
Seres Humanos
Leucemia Mieloide Aguda/patologia
Masculino
Proteínas Nucleares/genética
Valor Preditivo dos Testes
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (Biomarkers, Tumor); 0 (Nuclear Proteins); 117896-08-9 (nucleophosmin); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:161020
[Lr] Data última revisão:
161020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150214
[St] Status:MEDLINE
[do] DOI:10.1097/PDM.0000000000000034


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[PMID]:25637056
[Au] Autor:Bardet V; Wagner-Ballon O; Guy J; Morvan C; Debord C; Trimoreau F; Benayoun E; Chapuis N; Freynet N; Rossi C; Mathis S; Gourin MP; Toma A; Béné MC; Feuillard J; Guérin E; Groupe Francophone des Myélodysplasies (GFM); Groupe d'Etude Immunologique des Leucémies (GEIL)
[Ad] Endereço:Service d'Hématologie Biologique, Hôpitaux Universitaires Paris Centre-Cochin, Faculté de Médecine Paris Descartes, INSERM U1016, UMR 8104, Paris.
[Ti] Título:Multicentric study underlining the interest of adding CD5, CD7 and CD56 expression assessment to the flow cytometric Ogata score in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms.
[So] Source:Haematologica;100(4):472-8, 2015 Apr.
[Is] ISSN:1592-8721
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Although numerous recent publications have demonstrated interest in multiparameter flow cytometry in the investigation of myelodysplastic disorders, it is perceived by many laboratory hematologists as difficult and expensive, requiring a high level of expertise. We report a multicentric open real-life study aimed at evaluating the added value of the technically simple flow cytometry score described by the Ogata group for the diagnosis of myelodysplastic syndromes. A total of 652 patients were recruited prospectively in four different centers: 346 myelodysplastic syndromes, 53 myelodysplastic/myeloproliferative neoplasms, and 253 controls. The Ogata score was assessed using CD45 and CD34 staining, with the addition of CD10 and CD19. Moreover, labeling of CD5, CD7 and CD56 for the evaluation of myeloid progenitors and monocytes was tested on a subset of 294 patients. On the whole series, the specificity of Ogata score reached 89%. Respective sensitivities were 54% for low-risk myelodysplastic syndromes, 68% and 84% for type 1 and type 2 refractory anemia with excess of blasts, and 72% for myelodysplastic/myeloproliferative neoplasms. CD5 expression was poorly informative. When adding CD56 or CD7 labeling to the Ogata score, sensitivity rose to 66% for low-risk myelodysplastic syndromes, to 89% for myelodysplastic/myeloproliferative neoplasms and to 97% for refractory anemia with excess of blasts. This large multicenter study confirms the feasibility of Ogata scoring in routine flow cytometry diagnosis but highlights its poor sensitivity in low-risk myelodysplastic syndromes. The addition of CD7 and CD56 in flow cytometry panels improves the sensitivity but more sophisticated panels would be more informative.
[Mh] Termos MeSH primário: Antígenos CD7/metabolismo
Antígenos CD5/metabolismo
Antígeno CD56/metabolismo
Imunofenotipagem
Síndromes Mielodisplásicas/diagnóstico
Síndromes Mielodisplásicas/metabolismo
Doenças Mieloproliferativas-Mielodisplásicas/diagnóstico
Doenças Mieloproliferativas-Mielodisplásicas/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Antígenos CD7/genética
Antígenos CD5/genética
Antígeno CD56/genética
Diagnóstico Diferencial
Citometria de Fluxo
Expressão Gênica
Seres Humanos
Imunofenotipagem/métodos
Meia-Idade
Síndromes Mielodisplásicas/genética
Doenças Mieloproliferativas-Mielodisplásicas/genética
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (CD5 Antigens); 0 (CD56 Antigen)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150201
[St] Status:MEDLINE
[do] DOI:10.3324/haematol.2014.112755



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