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  1 / 20918 MEDLINE  
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[PMID]:29465554
[Au] Autor:Collinge E; Tigaud I; Balme B; Gerland LM; Sujobert P; Carlioz V; Salles G; Thomas X; Paubelle E
[Ad] Endereço:Department of Hematology, CHU UCL Namur, Belgium.
[Ti] Título:Case report: Purulent transformation of granulocytic sarcoma: An unusual pattern of differentiation in acute promyelocytic leukemia.
[So] Source:Medicine (Baltimore);97(8):e9657, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Acute promyelocytic leukemia (APL) is a curable subtype of acute myeloid leukemia. APL is currently treated with combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) resulting in the induction of apoptosis and differentiation of the leukemic cells. Differentiation syndrome (so-called ATRA syndrome) is the main life-threatening complication of induction therapy with these differentiating agents. PATIENT CONCERNS: Herein, we report the case of a 49-year-old woman diagnosed with APL with, concomitantly, a bulky cutaneous lesion of 10 cm diameter with a red-to-purple background and a necrotic center, localized on her abdomen. DIAGNOSES: After 10 days of treatment, the cutaneous lesion became purulent. Fluorescence in situ hybridization (FISH) analysis performed on this pus confirmed the presence of malignant features in the involved granulocytes proving their origin from the differentiation of leukemic APL cells, as all the analyzed nuclei showed 2 promyelocytic leukemia (PML)-retinoic acid receptor-a (RARA) fusions signals. INTERVENTION: The association by ATRA and ATO was continued. OUTCOME: Eventually, the evolution was favorable with healing in three weeks. LESSONS: This case report therefore highlights the differentiation phenomenon of promyelocytic blasts within promyelocytic sarcoma with the ATRA-ATO combination and the efficacy of this drug association in resolving both the malignant sarcoma and a secondary local infection.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Arsenicais/efeitos adversos
Leucemia Promielocítica Aguda/tratamento farmacológico
Óxidos/efeitos adversos
Sarcoma Mieloide/tratamento farmacológico
Tretinoína/efeitos adversos
[Mh] Termos MeSH secundário: Abdome/patologia
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Arsenicais/administração & dosagem
Diferenciação Celular/efeitos dos fármacos
Feminino
Seres Humanos
Quimioterapia de Indução/efeitos adversos
Meia-Idade
Óxidos/administração & dosagem
Sarcoma Mieloide/induzido quimicamente
Sarcoma Mieloide/patologia
Supuração/induzido quimicamente
Tretinoína/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenicals); 0 (Oxides); 5688UTC01R (Tretinoin); S7V92P67HO (arsenic trioxide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009657


  2 / 20918 MEDLINE  
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[PMID]:28456748
[Au] Autor:van Gils N; Verhagen HJMP; Smit L
[Ad] Endereço:Department of Hematology, VU University Medical Center, Cancer Center Amsterdam, Amsterdam, The Netherlands.
[Ti] Título:Reprogramming acute myeloid leukemia into sensitivity for retinoic-acid-driven differentiation.
[So] Source:Exp Hematol;52:12-23, 2017 08.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The success of all-trans retinoic acid (ATRA) therapy for acute promyelocytic leukemia (APL) provides a rationale for using retinoic acid (RA)-based therapy for other subtypes of acute myeloid leukemia (AML). Recently, several studies showed that ATRA may drive leukemic cells efficiently into differentiation and/or apoptosis in a subset of AML patients with an NPM1 mutation, a FLT3-ITD, an IDH1 mutation, and patients overexpressing EVI-1. Because not all patients within these molecular subgroups respond to ATRA and clinical trials that tested ATRA response in non-APL AML patients have had disappointing results, the identification of additional biomarkers may help to identify patients who strongly respond to ATRA-based therapy. Searching for response biomarkers might also reveal novel RA-based combination therapies with an efficient differentiation/apoptosis-inducing effect in non-APL AML patients. Preliminary studies suggest that the epigenetic or transcriptional state of leukemia cells determines their susceptibility to ATRA. We hypothesize that reprogramming by inhibitors of epigenetic-modifying enzymes or by modulation of microRNA expression might sensitize non-APL AML cells for RA-based therapy. AML relapse is caused by a subpopulation of leukemia cells, named leukemic stem cells (LSCs), which are in a different epigenetic state than the total bulk of the AML. The survival of LSCs after therapy is the main cause of the poor prognosis of AML patients, and novel differentiation therapies should drive these LSCs into maturity. In this review, we summarize the current knowledge on the epigenetic aspects of susceptibility to RA-induced differentiation in APL and non-APL AML.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Leucemia Mieloide/tratamento farmacológico
Tretinoína/uso terapêutico
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Doença Aguda
Antineoplásicos/uso terapêutico
Apoptose/genética
Diferenciação Celular/genética
Regulação Leucêmica da Expressão Gênica/efeitos dos fármacos
Histonas/metabolismo
Seres Humanos
Leucemia Mieloide/genética
Leucemia Mieloide/patologia
MicroRNAs/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Histones); 0 (MicroRNAs); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  3 / 20918 MEDLINE  
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[PMID]:29327472
[Au] Autor:He Y; Xu LL; Feng FE; Wang QM; Zhu XL; Wang CC; Zhang JM; Fu HX; Xu LP; Liu KY; Huang XJ; Zhang XH
[Ad] Endereço:Peking University People's Hospital, Peking University Institute of Haematology, Beijing, China.
[Ti] Título:Mesenchymal stem cell deficiency influences megakaryocytopoiesis through the TNFAIP3/NF-κB/SMAD pathway in patients with immune thrombocytopenia.
[So] Source:Br J Haematol;180(3):395-411, 2018 02.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Immune thrombocytopenia (ITP) is an autoimmune disease. Mesenchymal stem cells (MSCs) play important roles in the physiology and homeostasis of the haematopoietic system, including supporting megakaryocytic differentiation from CD34 haematopoietic progenitor cells. Tumour necrosis factor alpha-induced protein 3 (TNFAIP3, also termed A20) plays a key role in terminating NF-κB signalling. Human genetic studies showed that the polymorphisms of the TNFAIP3 gene may contribute to ITP susceptibility. In this study, we showed a significant decrease in TNFAIP3 and increase in NF-κB/SMAD7 in ITP-MSCs. In co-cultures with CD34 cells, NF-κB was overexpressed in MSCs from healthy controls (HC-MSCs) after transfection with NFKBIA (IκB)-specific short hairpin (sh)RNAs, resulting in MSC deficiency and a reduction in megakaryocytic differentiation and thrombopoiesis. Knockdown of TNFAIP3 expression using TNFAIP3-specific shRNAs in HC-MSCs affected megakaryocytopoiesis. However, IKBKB knockdown corrected megakaryocytopoiesis inhibition in the ITP-MSCs by decreasing NF-κB expression. Amplified TNFAIP3 expression in ITP-MSCs by TNFAIP3 cDNA can facilitate megakaryocyte differentiation. shRNA-mediated knockdown of SMAD7 expression rescued the impaired MSC function in ITP patients. Therefore, we demonstrate that a pathological reduction in TNFAIP3 levels induced NF-κB/SMAD7 pathway activation, causing a deficiency in MSCs in ITP patients. The ability of ITP-MSCs to support megakaryocytic differentiation and thrombopoiesis of CD34 cells was impaired.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/metabolismo
NF-kappa B/metabolismo
Púrpura Trombocitopênica Idiopática/etiologia
Púrpura Trombocitopênica Idiopática/metabolismo
Transdução de Sinais
Proteínas Smad/metabolismo
Trombopoese
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores
Medula Óssea/patologia
Estudos de Casos e Controles
Diferenciação Celular
Ensaio de Unidades Formadoras de Colônias
Citocinas/biossíntese
Expressão Gênica
Seres Humanos
Imunofenotipagem
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/patologia
Modelos Biológicos
NF-kappa B/genética
Púrpura Trombocitopênica Idiopática/diagnóstico
Púrpura Trombocitopênica Idiopática/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/genética
Trombopoese/efeitos dos fármacos
Trombopoese/genética
Fator de Crescimento Transformador beta/metabolismo
Tretinoína/farmacologia
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (NF-kappa B); 0 (Smad Proteins); 0 (Transforming Growth Factor beta); 5688UTC01R (Tretinoin); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.15034


  4 / 20918 MEDLINE  
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[PMID]:29225170
[Au] Autor:He MH; Zhang Q; Shu G; Lin JC; Zhao L; Liang XX; Yin L; Shi F; Fu HL; Yuan ZX
[Ad] Endereço:Department of Pharmacy, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan, 611130, China.
[Ti] Título:Dihydromyricetin sensitizes human acute myeloid leukemia cells to retinoic acid-induced myeloid differentiation by activating STAT1.
[So] Source:Biochem Biophys Res Commun;495(2):1702-1707, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The success of all-trans retinoic acid (ATRA) in differentiation therapy for patients with acute promyelocytic leukemia (APL) highly encourages researches to apply a new combination therapy based on ATRA. Therefore, research strategies to further sensitize cells to retinoids are urgently needed. In this study, we showed that Dihydromyricetin (DMY), a 2,3-dihydroflavonol compound, exhibited a strong synergy with ATRA to promote APL NB4 cell differentiation. We observed that DMY sensitized the NB4 cells to ATRA-induced cell growth inhibition, CD11b expression, NBT reduction and myeloid regulator expression. PML-RARα might not be essential for DMY-enhanced differentiation when combined with ATRA, while the enhanced differentiation was dependent on the activation of p38-STAT1 signaling pathway. Taken together, our study is the first to evaluate the synergy of DMY and ATRA in NB4 cell differentiation and to assess new opportunities for the combination of DMY and ATRA as a promising approach for future differentiation therapy.
[Mh] Termos MeSH primário: Flavonóis/administração & dosagem
Leucemia Promielocítica Aguda/tratamento farmacológico
Fator de Transcrição STAT1/metabolismo
Tretinoína/administração & dosagem
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sinergismo Farmacológico
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/metabolismo
Leucemia Mieloide Aguda/patologia
Leucemia Promielocítica Aguda/metabolismo
Leucemia Promielocítica Aguda/patologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteínas de Fusão Oncogênicas/metabolismo
Proteólise/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Flavonols); 0 (Oncogene Proteins, Fusion); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein); 5688UTC01R (Tretinoin); KD8QND6427 (dihydromyricetin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


  5 / 20918 MEDLINE  
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[PMID]:28470528
[Au] Autor:Kuenzel K; Mofrad SA; Gilbert DF
[Ad] Endereço:Institute of Medical Biotechnology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Paul-Gordan-Str. 3, 91052, Erlangen, Germany. Katharina.kuenzel@fau.de.
[Ti] Título:Phenotyping Cellular Viability by Functional Analysis of Ion Channels: GlyR-Targeted Screening in NT2-N Cells.
[So] Source:Methods Mol Biol;1601:205-214, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glycine receptor chloride channels (GlyRs) are attractive drug targets for therapeutic intervention and are also more and more recognized in the context of in vitro neurotoxicity and developmental neurotoxicity testing. Assaying the functional properties of GlyR can serve as an indicator of cellular viability and the integrity of the developing and mature central nervous system. Human pluripotent NTERA-2 (NT2) stem cells undergo neuronal differentiation upon stimulation with retinoic acid and express a large variety of neuronal proteins-including GlyR. YFP-I152L, a halide-sensitive variant of yellow fluorescent protein, allows high-throughput fluorescence-based functional analysis of GlyRs in NT2 cells. Here we describe a protocol for phenotyping of cellular viability by functional analysis of GlyR in neuronally differentiated NT2 (NT2-N) cells using YFP-I152L as a reporter of functional integrity of GlyRs. The protocol describes neuronal differentiation of NT2 stem cells, transient transfection of NT2-N cells with YFP-I152L as well as functional imaging and analysis of data from high-content imaging.
[Mh] Termos MeSH primário: Sobrevivência Celular
Células-Tronco de Carcinoma Embrionário/citologia
Neurogênese
Neurônios/citologia
Células-Tronco Pluripotentes/citologia
Receptores da Glicina/metabolismo
[Mh] Termos MeSH secundário: Diferenciação Celular
Avaliação Pré-Clínica de Medicamentos
Células-Tronco de Carcinoma Embrionário/efeitos dos fármacos
Seres Humanos
Proteínas Luminescentes/metabolismo
Neurogênese/efeitos dos fármacos
Imagem Óptica/métodos
Tretinoína/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Luminescent Proteins); 0 (Receptors, Glycine); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_16


  6 / 20918 MEDLINE  
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[PMID]:28470517
[Au] Autor:Menzner AK; Gilbert DF
[Ad] Endereço:Department of Internal Medicine 5, University Medical Center Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
[Ti] Título:A Protocol for In Vitro High-Throughput Chemical Susceptibility Screening in Differentiating NT2 Stem Cells.
[So] Source:Methods Mol Biol;1601:61-70, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incidence of neurological diseases including learning and developmental disorders has increased in recent years. Concurrently, the number and volume of worldwide registered and traded chemicals have also increased. There is a broad consensus that the developing brain is particularly sensitive to damage by chemicals and that evaluation of chemicals for developmental toxicity or neurotoxicity is critical to human health. Human pluripotent embryonal carcinoma (NTERA-2 or NT2) cells are increasingly considered as a suitable model for in vitro developmental toxicity and neurotoxicity (DT/DNT) studies as they undergo neuronal differentiation upon stimulation with retinoic acid (RA) and allow toxicity assessment at different stages of maturation. Here we describe a protocol for cell fitness screening in differentiating NT2 cells based on the analysis of intracellular ATP levels allowing for the identification of chemicals which are potentially harmful to the developing brain. The described method is suitable to be adapted to low-, medium-, and high-throughput screening and allows multiplexing with other cell fitness indicators. While the presented protocol focuses on cell fitness screening in human pluripotent stem cells it may also be applied to other in vitro models.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Encéfalo/embriologia
Sobrevivência Celular/efeitos dos fármacos
Células-Tronco de Carcinoma Embrionário/efeitos dos fármacos
Ensaios de Triagem em Larga Escala/métodos
Células-Tronco Pluripotentes/efeitos dos fármacos
Testes de Toxicidade
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Diferenciação Celular/efeitos dos fármacos
Avaliação Pré-Clínica de Medicamentos
Seres Humanos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Bibliotecas de Moléculas Pequenas/toxicidade
Tretinoína/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Small Molecule Libraries); 5688UTC01R (Tretinoin); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_5


  7 / 20918 MEDLINE  
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[PMID]:29374686
[Au] Autor:Song HY; Rellinger EJ; Park SH; Paul P; Qiao J; Vasilopoulos A; Ozden O; Gius D; Chung DH
[Ad] Endereço:Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical Center, Chicago, IL, U.S.A.
[Ti] Título:Inhibition of Sirtuin 6 Induces Neuroblastoma Differentiation.
[So] Source:Anticancer Res;38(2):647-654, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Sirtuins (SIRTs) play crucial roles in various signaling pathways that modulate differentiation and proliferation. We sought to elucidate the role of SIRTs in differentiation and proliferation of human neuroblastoma (NB). MATERIALS AND METHODS: NB cells were treated with nicotinamide (NAM), a non-specific SIRT inhibitor, SIRT-targeted short hairpin RNAs, and retinoic acid to assess cell growth and differentiation. RESULTS: SIRTs are involved in proliferation and differentiation using NAM in BE(2)-C cells. Specifically, SIRT6 knockdown in BE(2)-C cells reduced cell proliferation, induced neurite extension, corresponding with induction of p21 expression and G cell-cycle arrest. These effects were rescued by forced re-overexpression of SIRT6. SIRT6 expression was reduced in differentiated human NB sections, and RA-induced differentiation in BE(2)-C cells. CONCLUSION: SIRTs have important oncogenic properties in NB beyond its established functions in aging and genome stability. SIRT6 may represent a novel target for developing future therapeutics for the treatment of aggressive NBs.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Neuroblastoma/tratamento farmacológico
Neuroblastoma/metabolismo
Sirtuínas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Técnicas de Silenciamento de Genes
Seres Humanos
Neuroblastoma/patologia
Niacinamida/farmacologia
RNA Interferente Pequeno/farmacologia
Sirtuínas/genética
Tretinoína/administração & dosagem
Tretinoína/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 25X51I8RD4 (Niacinamide); 5688UTC01R (Tretinoin); EC 3.5.1.- (SIRT6 protein, human); EC 3.5.1.- (Sirtuins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  8 / 20918 MEDLINE  
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[PMID]:28461109
[Au] Autor:Amrouche K; Jamin C
[Ad] Endereço:UMR 1227, Lymphocytes B et Autoimmunité, Université de Brest, INSERM, Brest, France; LabEx IGO "Immunotherapy, Graft, Oncology", Brest, France.
[Ti] Título:Influence of drug molecules on regulatory B cells.
[So] Source:Clin Immunol;184:1-10, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:By their suppressive functions, regulatory B (Breg) cells are considered as key elements in the control and development of various disease states. Many signals can induce Bregs in vivo and in vitro and often from heterogeneous populations. Several specific signals delivered in a timely immunological context contribute to the establishment of Bregs. These are endogenous and physiological signals or stimuli, widely discussed in the literature participating in the establishment of an effective immune response. However, exogenous signals, much less clearly identified can also be considered as Bregs inducers. These extrinsic signals are capable of directly or indirectly influencing the suppressive capacity of Bregs, but also their expansion and functional restoration in its absence. Faced with the excitement generated by the development of processes favoring the expansion of Bregs in mice for therapeutic purposes, the challenge today is to extrapolate such approaches in humans. This perspective may already be in effect.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Linfócitos B Reguladores/efeitos dos fármacos
Imunossupressores/farmacologia
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Corticosteroides/farmacologia
Animais
Anticorpos Monoclonais Humanizados/farmacologia
Fator Ativador de Células B/imunologia
Linfócitos B Reguladores/imunologia
Antígenos CD40/imunologia
Citocinas/imunologia
Seres Humanos
Metotrexato/farmacologia
Ácido Micofenólico/farmacologia
Pirróis/farmacologia
Quinazolinas/farmacologia
Receptores de Antígenos de Linfócitos B/imunologia
Semaforinas/farmacologia
Sirolimo/farmacologia
Receptores Toll-Like/imunologia
Tretinoína/farmacologia
Vitamina D/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (B-Cell Activating Factor); 0 (CD40 Antigens); 0 (Cytokines); 0 (Immunosuppressive Agents); 0 (Pyrroles); 0 (Quinazolines); 0 (Receptors, Antigen, B-Cell); 0 (Semaphorins); 0 (Toll-Like Receptors); 0 (Vitamins); 1406-16-2 (Vitamin D); 5688UTC01R (Tretinoin); 7I279E1NZ8 (sotrastaurin); HU9DX48N0T (Mycophenolic Acid); I031V2H011 (tocilizumab); W36ZG6FT64 (Sirolimus); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  9 / 20918 MEDLINE  
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[PMID]:29186249
[Au] Autor:Sumita JM; Leonardi GR; Bagatin E
[Ad] Endereço:Dermatology Department of the Paulista Medical School - Universidade Federal de São Paulo (EPM - UNIFESP) - São Paulo (SP), Brazil.
[Ti] Título:Tretinoin peel: a critical view.
[So] Source:An Bras Dermatol;92(3):363-366, 2017 May-Jun.
[Is] ISSN:1806-4841
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The tretinoin peel, also known as retinoic acid peel, is a superficial peeling often performed in dermatological clinics in Brazil. The first study on this was published in 2001, by Cuce et al., as a treatment option for melasma. Since then, other studies have reported its applicability with reasonable methodology, although without a consistent scientific background and consensus. Topical tretinoin is used for the treatment of various dermatoses such as acne, melasma, scars, skin aging and non-melanoma skin cancer. The identification of retinoids cellular receptors was reported in 1987, but a direct cause-effect relation has not been established. This article reviews studies evaluating the use of topical tretinoin as agent for superficial chemical peel. Most of them have shown benefits in the treatment of melasma and skin aging. A better quality methodology in the study design, considering indication and intervention is indispensable regarding concentration, vehicle and treatment regimen (interval and number of applications). Additionally, more controlled and randomized studies comparing the treatment with tretinoin cream versus its use as a peeling agent, mainly for melasma and photoaging, are necessary.
[Mh] Termos MeSH primário: Abrasão Química/métodos
Ceratolíticos/administração & dosagem
Envelhecimento da Pele/efeitos dos fármacos
Dermatopatias/tratamento farmacológico
Tretinoína/administração & dosagem
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Keratolytic Agents); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:29199257
[Au] Autor:Yokota-Nakatsuma A
[Ad] Endereço:Laboratory of Immunology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University.
[Ti] Título:[Retinoic Acid Prevents Dendritic Cells from Inducing Novel Inflammatory T Cells That Produce Abundant Interleukin-13].
[So] Source:Yakugaku Zasshi;137(12):1491-1496, 2017.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Vitamin A (VA) plays critical roles in gut homeostasis. Dendritic cells in mesenteric lymph nodes (MLN-DCs) can metabolize VA to retinoic acid (RA), thereby inducing gut-tropic lymphocytes and enhancing peripheral differentiation of regulatory T cells expressing forkhead box P3. We found that MLN-DCs from VA-deficient mice induced a distinct inflammatory T helper type 2 (Th2)-cell subset that produced abundant interleukin-13 (IL-13) and expressed receptors for homing to skin and inflammatory sites but not to the intestine. IL-6-neutralizing antibodies or RA abrogated the induction of this subset. On the other hand, RA receptor antagonists allowed MLN-DCs from VA-sufficient mice to induce a similar T-cell subset. IL-6 induced the differentiation of this subset from naive CD4 T cells upon activation with antibodies against CD3 and CD28, and RA receptor antagonists enhanced this induction. It has been considered that VA deficiency reduces Th2-dependent antibody responses. However, oral administration of an antigen to VA-deficient mice failed to induce immune tolerance but primed strong IL-13-dependent immunoglobulin G1 (IgG1) responses and IgE responses that caused skin allergy. These results suggest that MLN-DCs possess the latent ability to induce IL-13-producing inflammatory Th2 cells and that RA prevents them from inducing IL-13-dependent allergic or inflammatory responses to orally administered antigens.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Interleucina-13/biossíntese
Células Th2/imunologia
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/imunologia
Hipersensibilidade/imunologia
Imunoglobulina E/imunologia
Imunoglobulina G/imunologia
Inflamação/imunologia
Interleucina-13/imunologia
Interleucina-6
Linfonodos/citologia
Mesentério
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (Interleukin-13); 0 (Interleukin-6); 37341-29-0 (Immunoglobulin E); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00153



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