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[PMID]:27772627
[Au] Autor:Razonable RR
[Ad] Endereço:Division of Infectious Diseases and the William J von Liebig Center for Transplantation and Clinical Regeneration, Mayo Clinic, Rochester, MN. Electronic address: razonable.raymund@mayo.edu.
[Ti] Título:Not the Usual Viral Suspects: Parvovirus B19, West Nile Virus, and Human T-Cell Lymphotrophic Virus Infections After Kidney Transplantation.
[So] Source:Semin Nephrol;36(5):428-434, 2016 09.
[Is] ISSN:1558-4488
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kidney transplant recipients are at increased risk of developing clinical disease due to uncommon opportunistic viral pathogens. Refractory anemia is classically associated with parvovirus B19 infection. West Nile virus has the propensity to cause fever and neurologic symptoms, while spastic paresis and lymphoma can be triggered by human T cell lymphotrophic virus. In this review article, the epidemiology, clinical manifestations, diagnosis and treatment of less common viruses are discussed in the setting of kidney transplantation.
[Mh] Termos MeSH primário: Eritema Infeccioso/induzido quimicamente
Rejeição de Enxerto/prevenção & controle
Infecções por HTLV-I/induzido quimicamente
Imunossupressores/efeitos adversos
Falência Renal Crônica/cirurgia
Transplante de Rim
Leucemia-Linfoma de Células T do Adulto/induzido quimicamente
Febre do Nilo Ocidental/induzido quimicamente
[Mh] Termos MeSH secundário: Antivirais/uso terapêutico
Eritema Infeccioso/diagnóstico
Eritema Infeccioso/terapia
Infecções por HTLV-I/diagnóstico
Infecções por HTLV-I/terapia
Seres Humanos
Leucemia-Linfoma de Células T do Adulto/diagnóstico
Leucemia-Linfoma de Células T do Adulto/terapia
Leucemia-Linfoma de Células T do Adulto/virologia
Paraparesia Espástica Tropical/induzido quimicamente
Paraparesia Espástica Tropical/diagnóstico
Paraparesia Espástica Tropical/terapia
Paraparesia Espástica Tropical/virologia
Infecções por Parvoviridae/induzido quimicamente
Infecções por Parvoviridae/diagnóstico
Infecções por Parvoviridae/terapia
Febre do Nilo Ocidental/diagnóstico
Febre do Nilo Ocidental/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Immunosuppressive Agents)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  2 / 3850 MEDLINE  
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Araújo, Marcelo Grossi
Texto completo SciELO Brasil
[PMID]:28954118
[Au] Autor:Oliveira LML; Souza MV; Guedes ACM; Araújo MG
[Ad] Endereço:Dermatology Service, Hospital das Clínicas, Universidade Federal de Minas Gerais - Belo Horizonte(MG), Brazil.
[Ti] Título:Case for diagnosis. Infective dermatitis associated with HTLV-1: differential diagnosis of atopic dermatitis.
[So] Source:An Bras Dermatol;92(4):573-574, 2017 Jul-Aug.
[Is] ISSN:1806-4841
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Infective dermatitis associated with HTLV-1 (IDH) is the main cutaneous marker of HTLV-1 infection. This disease occurs primarily in children and should be differentiated from other eczemas, especially from atopic dermatitis. The largest series of IDH are from Jamaica and Brazil. There are an estimated 15 to 20 million infected people in the world, and Brazil is one of the endemic regions. Studies suggest that IDH in children may be a marker for the development of T-cell leukemia/lymphoma (ATL) or myelopathy associated with HTLV-1/tropical spastic paraparesis (HAM / TSP) in adulthood.
[Mh] Termos MeSH primário: Dermatite/diagnóstico
Infecções por HTLV-I/diagnóstico
Dermatopatias Virais/diagnóstico
[Mh] Termos MeSH secundário: Dermatite/virologia
Dermatite Atópica/diagnóstico
Dermatite Atópica/virologia
Diagnóstico Diferencial
Eczema/diagnóstico
Eczema/virologia
Feminino
Infecções por HTLV-I/complicações
Seres Humanos
Leucemia-Linfoma de Células T do Adulto/diagnóstico
Dermatopatias Virais/complicações
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


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[PMID]:28910419
[Au] Autor:Sawada L; Nagano Y; Hasegawa A; Kanai H; Nogami K; Ito S; Sato T; Yamano Y; Tanaka Y; Masuda T; Kannagi M
[Ad] Endereço:Department of Immunotherapeutics, Tokyo Medical and Dental University, Graduate School of Medical and Dental Sciences, Bunkyo-ku, Tokyo, Japan.
[Ti] Título:IL-10-mediated signals act as a switch for lymphoproliferation in Human T-cell leukemia virus type-1 infection by activating the STAT3 and IRF4 pathways.
[So] Source:PLoS Pathog;13(9):e1006597, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type-1 (HTLV-1) causes two distinct diseases, adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Since there are no disease-specific differences among HTLV-1 strains, the etiological mechanisms separating these respective lymphoproliferative and inflammatory diseases are not well understood. In this study, by using IL-2-dependent HTLV-1-infected T-cell lines (ILTs) established from patients with ATL and HAM/TSP, we demonstrate that the anti-inflammatory cytokine IL-10 and its downstream signals potentially act as a switch for proliferation in HTLV-1-infected cells. Among six ILTs used, ILTs derived from all three ATL patients grew much faster than those from three HAM/TSP patients. Although most of the ILTs tested produced IFN-γ and IL-6, the production of IL-10 was preferentially observed in the rapid-growing ILTs. Interestingly, treatment with exogenous IL-10 markedly enhanced proliferation of the slow-growing HAM/TSP-derived ILTs. The IL-10-mediated proliferation of these ILTs was associated with phosphorylation of STAT3 and induction of survivin and IRF4, all of which are characteristics of ATL cells. Knockdown of STAT3 reduced expression of IL-10, implying a positive-feedback regulation between STAT3 and IL-10. STAT3 knockdown also reduced survivin and IRF4 in the IL-10- producing or IL-10- treated ILTs. IRF4 knockdown further suppressed survivin expression and the cell growth in these ILTs. These findings indicate that the IL-10-mediated signals promote cell proliferation in HTLV-1-infected cells through the STAT3 and IRF4 pathways. Our results imply that, although HTLV-1 infection alone may not be sufficient for cell proliferation, IL-10 and its signaling pathways within the infected cell itself and/or its surrounding microenvironment may play a critical role in pushing HTLV-1-infected cells towards proliferation at the early stages of HTLV-1 leukemogenesis. This study provides useful information for understanding of disease mechanisms and disease-prophylactic strategies in HTLV-1 infection.
[Mh] Termos MeSH primário: Proliferação Celular/fisiologia
Vírus 1 Linfotrópico T Humano
Interleucina-10/metabolismo
Leucemia-Linfoma de Células T do Adulto/imunologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Citocinas/metabolismo
Seres Humanos
Fatores Reguladores de Interferon/metabolismo
Paraparesia Espástica Tropical/imunologia
Fator de Transcrição STAT3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, human); 0 (Interferon Regulatory Factors); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (interferon regulatory factor-4); 130068-27-8 (Interleukin-10)
[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:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006597


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[PMID]:28866351
[Au] Autor:Sakihama S; Saito M; Kuba-Miyara M; Tomoyose T; Taira N; Miyagi T; Hayashi M; Kinjo S; Nakachi S; Tedokon I; Nishi Y; Tamaki K; Morichika K; Uchihara JN; Morishima S; Karube KN; Tanaka Y; Masuzaki H; Fukushima T
[Ad] Endereço:Laboratory of Hematoimmunology, Graduate School of Health Sciences, University of the Ryukyus, Nishihara, Japan.
[Ti] Título:Human T-cell leukemia virus type I Tax genotype analysis in Okinawa, the southernmost and remotest islands of Japan: Different distributions compared with mainland Japan and the potential value for the prognosis of aggressive adult T-cell leukemia/lymphoma.
[So] Source:Leuk Res;61:18-24, 2017 Oct.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Okinawa, comprising remote islands off the mainland of Japan, is an endemic area of human T-cell leukemia virus type I (HTLV-1), the causative virus of adult T-cell leukemia-lymphoma (ATL) and HTLV-1-associated myelopathy (HAM). We investigated the tax genotype of HTLV-1 among 29 HTLV-1 carriers, 74 ATL patients, and 33 HAM patients in Okinawa. The genotype distribution-60 (44%) taxA cases and 76 (56%) taxB cases-differed from that of a previous report from Kagoshima Prefecture in mainland Japan (taxA, 10%; taxB, 90%). A comparison of the clinical outcomes of 45 patients (taxA, 14; taxB, 31) with aggressive ATL revealed that the overall response and 1-year overall survival rates for taxA (50% and 35%, respectively) were lower than those for taxB (71% and 49%, respectively). In a multivariate analysis of two prognostic indices for aggressive ATL, Japan Clinical Oncology Group-Prognostic Index and Prognostic Index for acute and lymphoma ATL, with respect to age, performance status, corrected calcium, soluble interleukin-2 receptor, and tax genotype, the estimated hazard ratio of taxA compared with taxB was 2.68 (95% confidence interval, 0.87-8.25; P=0.086). Our results suggest that the tax genotype has clinical value as a prognostic factor for aggressive ATL.
[Mh] Termos MeSH primário: Produtos do Gene tax/genética
Infecções por HTLV-I/patologia
Leucemia-Linfoma de Células T do Adulto/patologia
Leucemia-Linfoma de Células T do Adulto/virologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Feminino
Genótipo
Infecções por HTLV-I/tratamento farmacológico
Infecções por HTLV-I/mortalidade
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
Japão
Estimativa de Kaplan-Meier
Leucemia-Linfoma de Células T do Adulto/mortalidade
Masculino
Meia-Idade
Reação em Cadeia da Polimerase
Polimorfismo de Fragmento de Restrição
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tax); 0 (tax protein, Human T-lymphotrophic virus 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170904
[St] Status:MEDLINE


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[PMID]:28776876
[Au] Autor:Ishida T; Utsunomiya A; Jo T; Yamamoto K; Kato K; Yoshida S; Takemoto S; Suzushima H; Kobayashi Y; Imaizumi Y; Yoshimura K; Kawamura K; Takahashi T; Tobinai K; Ueda R
[Ad] Endereço:Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
[Ti] Título:Mogamulizumab for relapsed adult T-cell leukemia-lymphoma: Updated follow-up analysis of phase I and II studies.
[So] Source:Cancer Sci;108(10):2022-2029, 2017 Oct.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The present study sought to elucidate the prognosis of adult T-cell leukemia-lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti-CCR4 monoclonal antibody. Progression-free survival (PFS) and overall survival (OS) of ATL patients enrolled in two studies are herein updated, namely NCT00355472 (phase I study of mogamulizumab in relapsed patients with ATL and peripheral T-cell lymphoma) and NCT00920790 (phase II study for relapsed ATL). Of 13 patients with relapsed aggressive ATL in the phase I study, four (31%) survived >3 years. For 26 relapsed patients with aggressive ATL in the phase II study, median PFS was 5.2 months and 1-year PFS was 26%, whereas median OS was 14.4 months, and 3-year OS was 23%. For patients without a rash or who developed a grade 1 rash only, median PFS was 0.8 months, and 1-year PFS was zero, with a median OS of 6.0 months, and 3-year OS of 8%. In contrast, for patients who developed a rash ≥grade 2, median PFS was 11.7 months, and 1-year PFS was 50%, with a median OS of 25.6 months, and 3-year OS of 36%. Thus, we conclude that mogamulizumab monotherapy may improve PFS and OS in some patients with relapsed aggressive ATL, especially those who develop a skin rash as a moderate immune-related adverse event. Therefore, further investigation is warranted to validate the present observations and to clarify the mechanisms involved in the activity of mogamulizumab.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/administração & dosagem
Leucemia-Linfoma de Células T do Adulto/tratamento farmacológico
Recidiva Local de Neoplasia/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Anticorpos Monoclonais Humanizados/uso terapêutico
Intervalo Livre de Doença
Feminino
Seres Humanos
Masculino
Meia-Idade
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); YI437801BE (mogamulizumab)
[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:170805
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13343


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[PMID]:28756726
[Au] Autor:Winsett FT; Lewis DJ; Duvic M
[Ad] Endereço:a University of Texas McGovern Medical School at Houston , Houston , TX , USA.
[Ti] Título:Mogamulizumab for the treatment of relapsed or refractory adult T-cell leukemia-lymphoma.
[So] Source:Expert Rev Hematol;10(9):757-760, 2017 Sep.
[Is] ISSN:1747-4094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Adult T-cell leukemia-lymphoma (ATL) is an aggressive variant of peripheral T-cell lymphoma of CD4+ T-malignant cells caused by human T-lymphotropic virus type-1. Despite aggressive treatment with multidrug combination chemotherapies, ATL confers a poor prognosis and commonly develops resistance to conventional treatments. Areas covered: Mogamulizumab is a humanized, defucosylated monoclonal antibody that acts by targeting the CC chemokine receptor 4 (CCR4) on malignant cells of ATL. In phase I and II clinical trials, it has achieved overall response rates of 31-50% in CCR4+ malignancies. The most commonly observed hematologic and non-hematologic adverse events included lymphocytopenia, neutropenia, leukocytopenia, infusion reaction, rash, and pyrexia. Expert commentary: Mogamulizumab has shown significant efficacy in treating ATL with moderately high response rates and has been approved in Japan for use in ATL. It may serve as a bridge therapy to achieve disease control prior to allogeneic hematopoietic stem cell transplantation. It also offers potential for use in combination with conventional chemotherapy. Determining the optimal combination of mogamulizumab with conventional and novel therapies remains an important strategy to improve the prognosis of patients with ATL.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Antineoplásicos/uso terapêutico
Leucemia-Linfoma de Células T do Adulto/tratamento farmacológico
Leucemia-Linfoma de Células T do Adulto/patologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/farmacologia
Citotoxicidade Celular Dependente de Anticorpos/imunologia
Antineoplásicos/farmacologia
Ensaios Clínicos como Assunto
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Leucemia-Linfoma de Células T do Adulto/imunologia
Leucemia-Linfoma de Células T do Adulto/mortalidade
Receptores CCR4/antagonistas & inibidores
Recidiva
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (Receptors, CCR4); YI437801BE (mogamulizumab)
[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:170801
[St] Status:MEDLINE
[do] DOI:10.1080/17474086.2017.1361819


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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]:28680001
[Au] Autor:Ishitsuka K
[Ad] Endereço:Kagoshima University Hospital, Department of Hematology and Immunology.
[Ti] Título:Progress in the management of ATL.
[So] Source:Rinsho Ketsueki;58(6):676-682, 2017.
[Is] ISSN:0485-1439
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Adult T-cell leukemia/lymphoma (ATL) is a peripheral T-cell malignancy caused by human T-lymphotropic virus type I (HTLV-1), and its prognosis remains poor. Three to five percent of HTLV-1 carriers, infected mainly by breast feeding, develop ATL after a latency period as long as 70 years. The standard of care for aggressive ATL and indolent ATL comprises intensive chemotherapy followed by allogeneic hematopoietic stem cell transplantation, if applicable, and watchful waiting, respectively. Outside Japan, a combination of interferon-α and zidovudine has also been used as a therapeutic option for acute, chronic, and smoldering-type ATLs. A Japanese nationwide retrospective study revealed the outcome of patients diagnosed between 2000 and 2009. The median survival times were 8.3, 10.6, 31.5, and 55.0 months and the 4-year overall survival rates were 11%, 16%, 36%, and 52% for acute, lymphoma, chronic, and smoldering-type ATLs, respectively. Recently, the development of several novel agents has been attempted by targeting surface antigens on ATL cells such as CCR4 and CD30 with monoclonal antibodies, targeting molecular abnormalities in ATL cells with EZH1/2 inhibitor, and modulating the immune environment via immunomodulatory drugs (IMiDs) or immune checkpoint inhibitors. Among them, a CCR4 monoclonal antibody mogamulizumab, and an IMiD, lenalidomide, have been introduced for clinical use in Japan.
[Mh] Termos MeSH primário: Leucemia-Linfoma de Células T do Adulto/terapia
[Mh] Termos MeSH secundário: Antígenos/imunologia
Seres Humanos
Leucemia-Linfoma de Células T do Adulto/diagnóstico
Leucemia-Linfoma de Células T do Adulto/imunologia
Leucemia-Linfoma de Células T do Adulto/mortalidade
Terapia de Alvo Molecular
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.11406/rinketsu.58.676


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[PMID]:28646117
[Au] Autor:Narita T; Ishida T; Ito A; Masaki A; Kinoshita S; Suzuki S; Takino H; Yoshida T; Ri M; Kusumoto S; Komatsu H; Imada K; Tanaka Y; Takaori-Kondo A; Inagaki H; Scholz A; Lienau P; Kuroda T; Ueda R; Iida S
[Ad] Endereço:Department of Hematology and Oncology and.
[Ti] Título:Cyclin-dependent kinase 9 is a novel specific molecular target in adult T-cell leukemia/lymphoma.
[So] Source:Blood;130(9):1114-1124, 2017 Aug 31.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyclin-dependent kinase 9 (CDK9), a subunit of the positive transcription elongation factor b (P-TEFb) complex, regulates gene transcription elongation by phosphorylating the C-terminal domain (CTD) of RNA polymerase II (RNAPII). The deregulation of CDK9/P-TEFb has important implications for many cancer types. BAY 1143572 is a novel and highly selective CDK9/P-TEFb inhibitor currently being investigated in phase 1 studies. We evaluated the therapeutic potential of BAY 1143572 in adult T-cell leukemia/lymphoma (ATL). As a result of CDK9 inhibition and subsequent inhibition of phosphorylation at serine 2 of the RNAPII CTD, BAY 1143572 decreased c-Myc and Mcl-1 levels in ATL-derived or human T-cell lymphotropic virus type-1 (HTLV-1)-transformed lines and primary ATL cells tested, leading to their growth inhibition and apoptosis. Median inhibitory concentrations for BAY 1143572 in ATL-derived or HTLV-1-transformed lines (n = 8), primary ATL cells (n = 11), and CD4 cells from healthy volunteers (n = 5) were 0.535, 0.30, and 0.36 µM, respectively. Next, NOG mice were used as recipients of tumor cells from an ATL patient. BAY 1143572-treated ATL-bearing mice (once daily 12.5 mg/kg oral application) demonstrated significantly decreased ATL cell infiltration of the liver and bone marrow, as well as decreased human soluble interleukin-2 receptor levels in serum (reflecting the ATL tumor burden), compared with untreated mice (n = 8 for both). BAY 1143572-treated ATL-bearing mice demonstrated significantly prolonged survival compared with untreated ATL-bearing mice (n = 7 for both). Collectively, this study indicates that BAY 1143572 showed strong potential as a novel treatment of ATL.
[Mh] Termos MeSH primário: Quinase 9 Dependente de Ciclina/antagonistas & inibidores
Leucemia-Linfoma de Células T do Adulto/enzimologia
Terapia de Alvo Molecular
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Medula Óssea/efeitos dos fármacos
Medula Óssea/patologia
Linhagem Celular Transformada
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Separação Celular
Quinase 9 Dependente de Ciclina/metabolismo
Vírus 1 Linfotrópico T Humano/fisiologia
Seres Humanos
Estimativa de Kaplan-Meier
Leucemia-Linfoma de Células T do Adulto/tratamento farmacológico
Leucemia-Linfoma de Células T do Adulto/patologia
Fígado/efeitos dos fármacos
Fígado/patologia
Camundongos
Inibidores de Proteínas Quinases/farmacocinética
Inibidores de Proteínas Quinases/farmacologia
Receptores de Interleucina-2/metabolismo
Transdução de Sinais/efeitos dos fármacos
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Receptors, Interleukin-2); EC 2.7.11.22 (Cyclin-Dependent Kinase 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-09-741983


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[PMID]:28627735
[Au] Autor:Kogure Y; Kataoka K
[Ad] Endereço:Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
[Ti] Título:Genetic alterations in adult T-cell leukemia/lymphoma.
[So] Source:Cancer Sci;108(9):1719-1725, 2017 Sep.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adult T-cell leukemia/lymphoma (ATL) is a peripheral T-cell neoplasm with a dismal prognosis. It is caused by human T-cell leukemia virus type-1 (HTLV-1) retrovirus. A long latency period from HTLV-1 infection to ATL onset suggests that not only HTLV-1 proteins, such as Tax and HBZ, but also additional genetic and/or epigenetic events are required for ATL development. Although many studies have demonstrated the biological functions of viral genes, alterations of cellular genes associated with ATL have not been fully investigated. Recently, a large-scale integrated genetic analysis revealed the entire landscape of somatic aberrations in ATL. This neoplasm is characterized by frequent gain-of-function alterations in components of the T-cell receptor/NF-κB signaling pathway, including activating mutations in the PLCG1, PRKCB, CARD11 and VAV1 genes, and CTLA4-CD28 and ICOS-CD28 fusions. Importantly, molecules associated with immune surveillance, such as HLA-A/B, CD58 and FAS, are affected recurrently. Among them, one notable lesion occurs as frequent structural variations that truncate the PD-L1 3'-untranslated region, leading to its overexpression. Other genetic targets include transcription factors (IRF4, IKZF2, and GATA3) and chemokine receptors (CCR4, CCR7 and GPR183), which are functionally relevant in normal T cells. A substantial proportion of ATL cases show widespread accumulation of repressive epigenetic changes, such as trimethylation of histone H3 lysine 27 and DNA hypermethylation of CpG islands, which coordinately modulate multiple pathways, including Cys2-His2 zinc finger genes involved in silencing retroelements. Here we review the current understanding of the genetic/epigenetic aberrations in ATL, focusing on their relevance in its molecular pathogenesis.
[Mh] Termos MeSH primário: Leucemia-Linfoma de Células T do Adulto/genética
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:170620
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13303



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