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  1 / 2546 MEDLINE  
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[PMID]:29061784
[Au] Autor:Ohtaka M; Itoh M; Tohda S
[Ad] Endereço:Department of Laboratory Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
[Ti] Título:BMI1 Inhibitors Down-regulate NOTCH Signaling and Suppress Proliferation of Acute Leukemia Cells.
[So] Source:Anticancer Res;37(11):6047-6053, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: B cell-specific Moloney murine leukemia virus integration site 1 (BMI1) is up-regulated in several cancers; therefore, we investigated the effects of BMI1 inhibitors on leukemia cells. MATERIALS AND METHODS: Four acute myeloid leukemia and two T-lymphoblastic leukemia cell lines were treated with BMI1 inhibitors artemisinin, PRT4165, and PTC-209 and analyzed for cell proliferation and gene expression by microarray and immunoblotting. RESULTS: PTC-209 and PRT4165 suppressed the growth of all cell lines through apoptosis.Artemisinin acted only on Jurkat cells. BMI1 inhibitors and BMI1-specific siRNA down-regulated the expression of NOTCH signaling proteins NOTCH1, HES1, and MYC. All but one cell lines did not have the cyclin-dependent kinase inhibitor 2A (CDKN2A) gene targeted by BMI1, thus the inhibitors acted through CDKN2A-independent pathways. CONCLUSION: BMI1 inhibition suppressed proliferation of leukemia cells through NOTCH signaling which functions downstream of BMI1, suggesting that BMI1 inhibitors can be candidate targeted drugs against leukemia.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Compostos Heterocíclicos com 2 Anéis/farmacologia
Leucemia Mieloide Aguda/patologia
Leucemia de Células T/patologia
Complexo Repressor Polycomb 1/antagonistas & inibidores
Receptores Notch/antagonistas & inibidores
Tiazóis/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/metabolismo
Leucemia de Células T/tratamento farmacológico
Leucemia de Células T/metabolismo
Complexo Repressor Polycomb 1/genética
Complexo Repressor Polycomb 1/metabolismo
RNA Interferente Pequeno/genética
Receptores Notch/genética
Receptores Notch/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMI1 protein, human); 0 (Heterocyclic Compounds, 2-Ring); 0 (PTC-209); 0 (RNA, Small Interfering); 0 (Receptors, Notch); 0 (Thiazoles); EC 2.3.2.27 (Polycomb Repressive Complex 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  2 / 2546 MEDLINE  
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[PMID]:28982851
[Au] Autor:Yang KJ; Piao L; Shin S; Shin SY; Li Y; Lee H; Tran Q; Park J; Hong S; Brazil DP; Hemmings BA; Kim SH; Park J
[Ad] Endereço:Metabolic Syndrome and Cell Signaling Laboratory, Department of Pharmacology and Medical Science, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
[Ti] Título:Modulation of PI3K/PTEN Pathway Does Not Affect Catalytic Activity of PDK1 in Jurkat Cells.
[So] Source:Anticancer Res;37(10):5415-5423, 2017 10.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Unopposed phosphoinositide 3-kinase (PI3K) activity and 3-phosphoinositide production in Jurkat cells, due to a mutation in the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) tumor-suppressor protein, results in deregulation of PH domain-containing proteins including the serine/threonine kinase PKB. In Jurkat cells, PKB is constitutively active and phosphorylated at the activation-loop residue (Thr308). 3-Phosphoinositide-dependent protein kinase-1 (PDK1), an enzyme that also contains a PH domain, catalyses Thr308 phosphorylation of PKB in addition to other kinase families such as PKC isoforms. It is unknown, however, whether the loss of PTEN in Jurkat cells also results in unregulated PDK1 activity and whether such loss has an impact on activation-loop phosphorylation of other PDK1 substrates e.g. PKC. In this study, we addressed whether loss of PTEN in Jurkat cells affects PDK1 catalytic activity and intracellular localization. We demonstrated that reducing the level of 3-phosphoinositides in Jurkat cells with pharmacological inhibitors of PI3K or expression of PTEN does not affect PDK1 activity or its intracellular localization. We conclude, therefore, that although Jurkat cells lack PTEN expression, only a subset of pathways downstream of PDK1 are perturbed as a consequence of PTEN loss.
[Mh] Termos MeSH primário: Proteínas Quinases Dependentes de 3-Fosfoinositídeo/metabolismo
Leucemia de Células T/enzimologia
PTEN Fosfo-Hidrolase/metabolismo
Fosfatidilinositol 3-Quinase/metabolismo
[Mh] Termos MeSH secundário: Catálise
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células Jurkat
Leucemia de Células T/genética
Leucemia de Células T/patologia
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinase/antagonistas & inibidores
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RETRACTED PUBLICATION
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (3-Phosphoinositide-Dependent Protein Kinases); EC 2.7.11.1 (PDPK1 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


  3 / 2546 MEDLINE  
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[PMID]:28832644
[Au] Autor:Mitsuhashi Y; Furusawa Y; Aradate T; Zhao QL; Moniruzzaman R; Kanamori M; Noguchi K; Kondo T
[Ad] Endereço:Department of Radiological Sciences, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Sugitani, Toyama, Japan.
[Ti] Título:3-O-trans-p-coumaroyl-alphitolic acid, a triterpenoid from Zizyphus jujuba, leads to apoptotic cell death in human leukemia cells through reactive oxygen species production and activation of the unfolded protein response.
[So] Source:PLoS One;12(8):e0183712, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:3-O-trans-p-coumaroyl-alphitolic acid (3OTPCA), a triterpenoid isolated from the plant Zizyphus jujuba (ZJ), is known to be cytotoxic to cancer cells; however, the molecular mechanism underlying 3OTPCA-induced cell death remains unknown. Here, we provide novel evidence that 3OTPCA induces apoptotic cell death in human leukemia cells. We found that 3OPTCA induces DNA fragmentation within 24 h after treatment in U937 cells, which was also observed in other leukemia cell lines, including Molt-4 and Jurkat cells. We then investigated other parameters involved in apoptosis, including phosphatidylserine externalization and caspase-3 cleavage in U937 cells treated with 3OTPCA. 3OTPCA caused significant DNA fragmentation, annexin-V binding, and caspase-3 cleavage, indicating that 3OTPCA exerts cytotoxicity through apoptosis induction. RNA-seq analysis revealed that the expression of transcripts associated with the unfolded protein response (UPR), such as spliced XBP-1 and CHOP, were up-regulated by 3OTPCA treatment. 3OTPCA-induced UPR activation may be due to endoplasmic reticulum (ER) stress because both 3OTPCA and thapsigargin, an endoplasmic Ca2+ transport ATPase inhibitor, increased intracellular calcium levels. 3OTPCA down-regulated the expression of Bcl-2, a target of CHOP, and led to the loss of the mitochondrial membrane, indicating that the intrinsic (mitochondrial) apoptotic pathway was triggered by 3OTPCA, likely through UPR activation. Furthermore, we found that 3OTPCA induced superoxide anion generation and, following p38 MAPK phosphorylation, caspase-8 cleavage without affecting Fas expression. It also induced subsequent Bid cleavage, which may enhance the apoptosis triggered by the intrinsic pathway. These findings reveal for the first time that 3OTPCA induces apoptotic cell death through the generation of reactive oxygen species and activation of UPR.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Leucemia de Células T/patologia
Espécies Reativas de Oxigênio/metabolismo
Triterpenos/farmacologia
Resposta a Proteínas não Dobradas
Ziziphus/química
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Cálcio/metabolismo
Ativação Enzimática
Seres Humanos
Células Jurkat
Leucemia de Células T/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-O-p-coumaroylalphitolic acid); 0 (Biomarkers); 0 (Reactive Oxygen Species); 0 (Triterpenes); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183712


  4 / 2546 MEDLINE  
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[PMID]:28543380
[Au] Autor:Perera LP; Zhang M; Nakagawa M; Petrus MN; Maeda M; Kadin ME; Waldmann TA; Perera PY
[Ad] Endereço:Lymphoid Malignancies Branch, National Cancer Institute, Bethesda, Maryland, 20892-1374, USA.
[Ti] Título:Chimeric antigen receptor modified T cells that target chemokine receptor CCR4 as a therapeutic modality for T-cell malignancies.
[So] Source:Am J Hematol;92(9):892-901, 2017 Sep.
[Is] ISSN:1096-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:With the emerging success of treating CD19 expressing B cell malignancies with ex vivo modified, autologous T cells that express CD19-directed chimeric antigen receptors (CAR), there is intense interest in expanding this evolving technology to develop effective modalities to treat other malignancies including solid tumors. Exploiting this approach to develop a therapeutic modality for T cell malignancies for which the available regimens are neither curative, nor confer long term survival we generated a lentivirus-based CAR gene transfer system to target the chemokine receptor CCR4 that is over-expressed in a spectrum of T cell malignancies as well as in CD4 CD25 Foxp3 T regulatory cells that accumulate in the tumor microenvironment constituting a barrier against anti-tumor immunity. Ex vivo modified, donor-derived T cells that expressed CCR4 directed CAR displayed antigen-dependent potent cytotoxicity against patient-derived cell lines representing ATL, CTCL, ALCL and a subset of HDL. Furthermore, these CAR T cells also eradicated leukemia in a mouse xenograft model of ATL illustrating the potential utility of this modality in the treatment of a wide spectrum of T cell malignancies.
[Mh] Termos MeSH primário: Neoplasias Hematológicas
Receptores de Antígenos de Linfócitos T
Receptores CCR4/antagonistas & inibidores
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Neoplasias Hematológicas/genética
Neoplasias Hematológicas/imunologia
Neoplasias Hematológicas/patologia
Neoplasias Hematológicas/terapia
Seres Humanos
Leucemia de Células T/genética
Leucemia de Células T/imunologia
Leucemia de Células T/patologia
Leucemia de Células T/terapia
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T/imunologia
Receptores CCR4/genética
Receptores CCR4/imunologia
Linfócitos T Reguladores/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCR4 protein, human); 0 (Receptors, Antigen, T-Cell); 0 (Receptors, CCR4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1002/ajh.24794


  5 / 2546 MEDLINE  
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[PMID]:28361854
[Au] Autor:Kit Y; Magorivska I; Bilyi R; Myronovskij S; Stoika R
[Ad] Endereço:Institute of Cell Biology, National Academy of Sciences of Ukraine, Lviv 79005, Ukraine.
[Ti] Título:Anti-histone H1 IgGs possess proliferative activity towards human T-leukaemia CEM cells.
[So] Source:Exp Oncol;39(1):36-41, 2017 Mar.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to characterize the proliferative activity of the anti-histone H1 IgGs towards human T-leukaemia CEM cells. MATERIALS AND METHODS: Anti-histone H1 IgGs were purified from blood serum of systemic lupus erythematosus patients by precipitation of serum proteins with 50% ammonium sulfate followed by a sequential affinity chromatography on Protein G-Sepharose and histone H1-Sepharose columns. To avoid contamination with other proteins, anti-histone H1 IgGs were subjected to strongly acidic pH 2.0 during gel filtration through HPLC column. The effects of the anti-histone H1 IgGs on cell viability and cell cycle were tested by MTS-assay and flow cytometry, correspondingly. The cross-reactivity of the anti-histone H1 antibodies towards heterogenetic and cellular antigens was evaluated by Western-blot analysis. RESULTS: It was found that incubation of CEM cells with the HPLC-purified anti-histone H1 IgGs resulted in significant stimulation of cell growth by 46% after 48 h of incubation. These IgGs possess an antigenic poly-specificity to positively charged heterogenetic antigens and different cellular antigens. FITC-labeled and biotinylated anti-histone H1 IgGs are internalized by CEM cells and preferentially accumulated in the cytoplasm. CONCLUSION: The anti-histone H1 IgGs are shown to internalize human T-leukemia CEM and stimulate their proliferation. These IgGs are polyspecific toward cellular antigens.
[Mh] Termos MeSH primário: Anticorpos Anti-Idiotípicos/farmacologia
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Histonas/imunologia
[Mh] Termos MeSH secundário: Anticorpos Anti-Idiotípicos/isolamento & purificação
Anticorpos Anti-Idiotípicos/metabolismo
Afinidade de Anticorpos/imunologia
Especificidade de Anticorpos/imunologia
Western Blotting
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Cromatografia de Afinidade
Cromatografia em Gel
Reações Cruzadas/imunologia
Citoplasma/metabolismo
Seres Humanos
Leucemia de Células T/imunologia
Leucemia de Células T/metabolismo
Leucemia de Células T/patologia
Lúpus Eritematoso Sistêmico/sangue
Lúpus Eritematoso Sistêmico/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Anti-Idiotypic); 0 (Histones); 0 (anti-IgG)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170628
[Lr] Data última revisão:
170628
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE


  6 / 2546 MEDLINE  
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[PMID]:28223690
[Au] Autor:Zhu X; Duan Y; Cui Z; Wang Z; Li Z; Zhang Y; Ju J; Huang H
[Ad] Endereço:Xiangya International Academy of Translational Medicine, Central South University, National Engineering Research Center of Combinatorial Biosynthesis for Drug Discovery, Changsha, China.
[Ti] Título:Cytotoxic rearranged angucycline glycosides from deep sea-derived Streptomyces lusitanus SCSIO LR32.
[So] Source:J Antibiot (Tokyo);70(7):819-822, 2017 Jul.
[Is] ISSN:0021-8820
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Two new rearranged linear angucycline glycosides, designated grincamycins G and H (1 and 2), together with three known congers P-1894B (vineomycin A , 3), saquayamycin B (4) and vineomycin B (5), were obtained from marine-derived actinomycete Streptomyces lusitanus SCSIO LR32. The structures of 1 and 2 were elucidated by MS, 1D and 2D NMR techniques. Compounds 2-5 showed significant inhibitory effect on Jurkat T-cell proliferation with IC values of 3.0, 0.011, 0.037 and 0.3 µM, respectively.
[Mh] Termos MeSH primário: Antraquinonas/isolamento & purificação
Antineoplásicos/isolamento & purificação
Glicosídeos/isolamento & purificação
Streptomyces/metabolismo
[Mh] Termos MeSH secundário: Antraquinonas/química
Antraquinonas/farmacologia
Antineoplásicos/química
Antineoplásicos/farmacologia
Proliferação Celular/efeitos dos fármacos
Glicosídeos/química
Glicosídeos/farmacologia
Seres Humanos
Concentração Inibidora 50
Células Jurkat
Leucemia de Células T/tratamento farmacológico
Leucemia de Células T/patologia
Espectroscopia de Ressonância Magnética
Espectrometria de Massas
Streptomyces/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Antineoplastic Agents); 0 (Glycosides)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1038/ja.2017.17


  7 / 2546 MEDLINE  
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[PMID]:28115371
[Au] Autor:Marks DI; Rowntree C
[Ad] Endereço:Adult Bone Marrow Transpant Unit, University Hospitals Bristol National Health Service Foundation Trust, Bristol, United Kingdom; and Department of Haematology, University Hospital of Wales, Cardiff, United Kingdom.
[Ti] Título:Management of adults with T-cell lymphoblastic leukemia.
[So] Source:Blood;129(9):1134-1142, 2017 Mar 02.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T-cell acute lymphoblastic leukemia (ALL) is a rare disease in adults with inferior survival outcomes compared with those seen in pediatric patients. Although potentially curable with ∼50% survival at 5 years, adult patients with relapsed disease have dismal outcomes with <10% of patients surviving long term. This review will discuss the diagnosis and management of adult patients with newly diagnosed T-cell ALL with an emphasis on the immunophenotypic and genetic analyses required to assign prognosis, risk stratify, and guide post-remission therapy. The evidence for the main components of complex T-cell ALL treatment regimens is described. The importance of monitoring minimal residual disease is emphasized, with a discussion of the different methods used. The results of hematopoietic cell transplantation are analyzed, and recommendations made about which patients should be considered for this intervention. The treatment of the adolescent and young adult group is delineated, and the role of using "pediatric-inspired" regimens in older adults considered. We also describe the current data and potential future options for the use of novel therapies, including nelarabine and γ-secretase inhibitors, in adult patients with T-cell ALL.
[Mh] Termos MeSH primário: Leucemia de Células T/diagnóstico
Leucemia de Células T/terapia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Seres Humanos
Leucemia de Células T/genética
Masculino
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-07-692608


  8 / 2546 MEDLINE  
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[PMID]:28087047
[Au] Autor:Mazor R; Kaplan G; Park D; Jang Y; Lee F; Kreitman R; Pastan I
[Ad] Endereço:Laboratory of Molecular Biology, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892-4264, USA. Electronic address: mazorr@mail.nih.gov.
[Ti] Título:Rational design of low immunogenic anti CD25 recombinant immunotoxin for T cell malignancies by elimination of T cell epitopes in PE38.
[So] Source:Cell Immunol;313:59-66, 2017 Mar.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:LMB-2, is a potent recombinant immunotoxin (RIT) that is composed of scFv antibody that targets CD25 (Tac) and a toxin fragment (PE38). It is used to treat T cell leukemias and lymphomas. To make LMB-2 less immunogenic, we introduced a large deletion in domain II and six point mutations in domain III that were previously shown to reduce T cell activation in other RITs. We found that unlike other RITs, deletion of domain II from LMB-2 severely compromised its activity. Rather than deletion, we identified T cell epitopes in domain II and used alanine substitutions to identify point mutations that diminished those epitopes. The novel RIT, LMB-142 contains a 38kDa toxin and nine point mutations that diminished T cell response to the corresponding peptides by an average of 75%. LMB-142 has good cytotoxic activity and has lower nonspecific toxicity in mice. LMB-142 should be more efficient in cancer therapy because more treatment cycles can be given.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Imunoterapia/métodos
Imunotoxinas/uso terapêutico
Leucemia de Células T/terapia
Pseudomonas/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/genética
Toxinas Bacterianas/genética
Linhagem Celular Tumoral
Proliferação Celular
Citocinas/metabolismo
Desenho de Drogas
ELISPOT
Epitopos de Linfócito T/genética
Exotoxinas/genética
Exotoxinas/uso terapêutico
Feminino
Engenharia Genética
Seres Humanos
Imunotoxinas/genética
Subunidade alfa de Receptor de Interleucina-2/imunologia
Leucemia de Células T/imunologia
Ativação Linfocitária
Camundongos
Mutagênese Sítio-Dirigida
Mutação/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (B3(Fv)-PE38KDEL recombinant immunotoxin); 0 (Bacterial Toxins); 0 (Cytokines); 0 (Epitopes, T-Lymphocyte); 0 (Exotoxins); 0 (Immunotoxins); 0 (Interleukin-2 Receptor alpha Subunit)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE


  9 / 2546 MEDLINE  
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[PMID]:28083948
[Au] Autor:Cedeno-Laurent F; Wysocka M; Obstfeld AE; Novoa RA; Vittorio CC; Kim EJ; Weng WK; Rook AH
[Ad] Endereço:Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
[Ti] Título:Gain of CD26 expression on the malignant T-cells in relapsed erythrodermic leukemic mycosis fungoides.
[So] Source:J Cutan Pathol;44(5):462-466, 2017 May.
[Is] ISSN:1600-0560
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loss of CD26 surface expression on the circulating malignant T-cell is the most widely accepted diagnostic marker in patients with leukemic cutaneous T-cell lymphoma (CTCL). CTCL cases with reemergence of CD7 and/or CD26 surface expression are unusual and of uncertain prognosis. We report the case of an erythrodermic leukemic mycosis fungoides patient who had achieved temporary remission after several months on multimodality immunotherapy and extracorporeal photopheresis, but who relapsed with aggressive disease phenotypically characterized by CD4+ T-cells with high CD26 expression. Polymerase chain reaction studies and high-throughput sequencing analyses from peripheral blood mononuclear cells at presentation and relapse consistently showed an identical clonal T-cell receptor suggesting evolution of her original malignant clone which lacked CD26 expression. Interestingly, quantitative expression of the sialomucin, CD164, mirrored her clinical picture, thus favoring its reliability as a novel biomarker in CTCL.
[Mh] Termos MeSH primário: Biomarcadores Tumorais
Linfócitos T CD4-Positivos
Dermatite Esfoliativa
Dipeptidil Peptidase 4/biossíntese
Regulação Enzimológica da Expressão Gênica
Regulação Leucêmica da Expressão Gênica
Leucemia de Células T
Micose Fungoide
Proteínas de Neoplasias/biossíntese
Neoplasias Cutâneas
[Mh] Termos MeSH secundário: Idoso
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD4-Positivos/patologia
Dermatite Esfoliativa/metabolismo
Dermatite Esfoliativa/patologia
Feminino
Seres Humanos
Leucemia de Células T/metabolismo
Leucemia de Células T/patologia
Micose Fungoide/metabolismo
Micose Fungoide/patologia
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neoplasm Proteins); EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1111/cup.12899


  10 / 2546 MEDLINE  
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[PMID]:28060797
[Au] Autor:Gattinoni L; Speiser DE; Lichterfeld M; Bonini C
[Ad] Endereço:Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
[Ti] Título:T memory stem cells in health and disease.
[So] Source:Nat Med;23(1):18-27, 2017 Jan 06.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T memory stem (T ) cells are a rare subset of memory lymphocytes endowed with the stem cell-like ability to self-renew and the multipotent capacity to reconstitute the entire spectrum of memory and effector T cell subsets. Cumulative evidence in mice, nonhuman primates and humans indicates that T cells are minimally differentiated cells at the apex of the hierarchical system of memory T lymphocytes. Here we describe emerging findings demonstrating that T cells, owing to their extreme longevity and robust potential for immune reconstitution, are central players in many physiological and pathological human processes. We also discuss how T cell stemness could be leveraged therapeutically to enhance the efficacy of vaccines and adoptive T cell therapies for cancer and infectious diseases or, conversely, how it could be disrupted to treat T cell driven and sustained diseases, such as autoimmunity, adult T cell leukemia and HIV-1.
[Mh] Termos MeSH primário: Autorrenovação Celular/imunologia
Memória Imunológica/imunologia
Células-Tronco/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Doenças Autoimunes/imunologia
Doenças Autoimunes/terapia
Diferenciação Celular
Infecções por HIV/imunologia
Infecções por HIV/terapia
Seres Humanos
Leucemia de Células T/imunologia
Leucemia de Células T/terapia
Linfócitos T/transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4241



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