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1. Leucemia de células T do adulto Adult T-cell leukemia

Author

Heike Brand, João Guilherme B. Alves, Francisco Pedrosa, and Norma Lucena-Silva

Subjects
Leucemia, HTLV-1, ATL, Leukemia, Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

A leucemia de células T no adulto (ATL) é causada pelo vírus linfotrópico de células T (HTLV-1). Contudo, apenas 2%-5% dos indivíduos infectados desenvolvem a ATL e somente 40-60 anos após a infecção. Um fator de risco para adquirir a doença é a via da transmissão do vírus pela amamentação e durante o parto, sugerindo que a criança já é portadora do vírus. Desde a descoberta do vírus, em 1980, vários artigos científicos foram publicados descrevendo as manifestações clínicas, biologia do vírus e alterações intracelulares induzidas pelo vírus. Esta revisão visa explorar alguns aspectos da relação entre HTLV-1 e a leucemia de células T do Adulto.The human T-lymphotropic virus (HTLV-1) is known to be the etiologic agent of adult T-cell leukemia (ATL). Only 2-5% of infected individuals develop ATL and even then only 40-60 years after infection. One risk factor to develop ATL is the transmission of the virus by breastfeeding and during delivery, suggesting that infants of infected mothers are already carriers of the virus. Since the discovery of the virus in 1980 many scientific papers have been published describing the clinical manifestations, biology of the virus and the intracellular alterations induced by the virus. This review aims to explore some aspects of the relationship between HTLV-1 and ATL.

Published
2009

2. Estrogen Receptor-α Directs Ordered, Cyclical, and Combinatorial Recruitment of Cofactors on a Natural Target Promoter

Author

Heike Brand, Raphaël Métivier, Martin Kos, Frank Gannon, Graziella Penot, Michael R Hübner, and George Reid

Subjects
Transcriptional Activation, Biology, General Biochemistry, Genetics and Molecular Biology, Chromatin remodeling, Histone Deacetylases, Epigenesis, Genetic, 03 medical and health sciences, 0302 clinical medicine, Biological Clocks, Cell Line, Tumor, Histone code, Humans, Promoter Regions, Genetic, Transcription factor, ChIA-PET, 030304 developmental biology, Genetics, 0303 health sciences, General transcription factor, Biochemistry, Genetics and Molecular Biology(all), Tumor Suppressor Proteins, Pioneer factor, Estrogen Receptor alpha, Proteins, Estrogens, Chromatin, Cell biology, Nucleosomes, Receptors, Estrogen, 030220 oncology & carcinogenesis, Trefoil Factor-1, Chromatin immunoprecipitation
Abstract

Transcriptional activation of a gene involves an orchestrated recruitment of components of the basal transcription machinery and intermediate factors, concomitant with an alteration in local chromatin structure generated by posttranslational modifications of histone tails and nucleosome remodeling. We provide here a comprehensive picture of events resulting in transcriptional activation of a gene, through evaluating the estrogen receptor-α (NR3A1) target pS2 gene promoter in MCF-7 cells. This description integrates chromatin remodeling with a kinetic evaluation of cyclical networks of association of 46 transcription factors with the promoter, as determined by chromatin immunoprecipitation assays. We define the concept of a "transcriptional clock" that directs and achieves the sequential and combinatorial assembly of a transcriptionally productive complex on a promoter. Furthermore, the unanticipated findings of key roles for histone deacetylases and nucleosome-remodeling complexes in limiting transcription implies that transcriptional activation is a cyclical process that requires both activating and repressive epigenetic processes.

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