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1.
Br J Dermatol ; 175(4): 782-4, 2016 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26875995

RESUMO

Graft-versus-host disease-associated angiomatosis (GVHD-AA) is an uncommon manifestation of chronic GVHD consisting of friable vascular proliferations. Using fluorescence in situ hybridization, we demonstrate the presence of donor-derived endothelial cells within areas of GVHD-AA. This is the first documented occurrence of a benign neoplastic growth in relationship to a form of chronic GVHD.


Assuntos
Angiomatose/etiologia , Doença Enxerto-Hospedeiro/etiologia , Transplante de Células-Tronco Hematopoéticas/efeitos adversos , Escleroderma Sistêmico/etiologia , Quimeras de Transplante , Quimera , Doença Crônica , Células Endoteliais , Feminino , Humanos , Cromossomos Sexuais , Transplante Homólogo
2.
Leukemia ; 27(4): 871-8, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23178755

RESUMO

Histone deacetylase (HDAC) inhibitors either alone or in combination with hypomethylating agents have limited clinical effect in acute myeloid leukemia (AML). Previously, we demonstrated that AML patients with higher miR (microRNA)-29b expression had better response to the hypomethylating agent decitabine. Therefore, an increase in miR-29b expression preceding decitabine treatment may provide a therapeutic advantage. We previously showed that miR-29b expression is suppressed by a repressor complex that includes HDACs. Thus, HDAC inhibition may increase miR-29b expression. We hypothesized that priming AML cells with the novel HDAC inhibitor (HDACI) AR-42 would result in increased response to decitabine treatment via upregulation of miR-29b. Here, we show that AR-42 is a potent HDACI in AML, increasing miR-29b levels and leading to downregulation of known miR-29b targets (that is, SP1, DNMT1, DNMT3A and DNMT3B). We then demonstrated that the sequential administration of AR-42 followed by decitabine resulted in a stronger anti-leukemic activity in vitro and in vivo than decitabine followed by AR-42 or either drug alone. These preclinical results with AR-42 priming before decitabine administration represent a promising, novel treatment approach and a paradigm shift with regard to the combination of epigenetic-targeting compounds in AML, where decitabine has been traditionally given before HDACIs.


Assuntos
Azacitidina/análogos & derivados , Epigênese Genética , Inibidores de Histona Desacetilases/uso terapêutico , Leucemia Mieloide Aguda/tratamento farmacológico , MicroRNAs/genética , Fenilbutiratos/uso terapêutico , Animais , Azacitidina/uso terapêutico , Western Blotting , Linhagem Celular Tumoral , Decitabina , Histona Desacetilases/metabolismo , Humanos , Leucemia Mieloide Aguda/enzimologia , Leucemia Mieloide Aguda/genética , Camundongos , Camundongos Endogâmicos NOD , Camundongos SCID , Regulação para Cima/efeitos dos fármacos
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