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Nicole D. Facompre Pavithra Rajagopalan Varun Sahu Alexander T. Pearson Kathleen T. Montone Claire D. James Frederico O. Gleber-Netto Gregory S. Weinstein Jalal Jalaly Alexander Lin Anil K. Rustgi Hiroshi Nakagawa Joseph A. Califano Curtis R. Pickering Elizabeth A. White Bradford E. Windle Iain M. Morgan Roger B. Cohen Phyllis A. Gimotty Devraj Basu 《International journal of cancer. Journal international du cancer》2020,147(11):3236-3249
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Primary cutaneous anaplastic large cell lymphomas with 6p25.3 rearrangement exhibit particular histological features 下载免费PDF全文
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Dalton Luiz Schiessel Ricardo K. Yamazaki Marcelo Kryczyk Isabela Coelho de Castro Adriana A. Yamaguchi Danielle C. T. Pequito 《Nutrition and cancer》2016,68(8):1369-1380
Objective: Polyunsaturated fatty acids n-3 (PUFA n-3) have shown effects in reducing tumor growth, in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) abundantly present in fish oil (FO). When these fatty acids are provided in the diet, they alter the functions of the cells, particularly in tumor and immune cells. However, the effects of α-linolenic fatty acid (ALA), which is the precursor of EPA and DHA, are controversial. Thus, our objective was to test the effect of this parental fatty acid. Methods: Non-tumor-bearing and tumor-bearing Wistar rats (70 days) were supplemented with 1 g/kg body weight of FO or Oro Inca® (OI) oil (rich in ALA). Immune cells function, proliferation, cytokine production, and subpopulation profile were evaluated. Results: We have shown that innate immune cells enhanced phagocytosis capacity, and increased processing and elimination of antigens. Moreover, there was a decrease in production of pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6)) by macrophages. Lymphocytes showed decreased proliferation capacity, increased cluster of differentiation 8 (CD8+) subpopulation, and increased TNF-α production. Conclusions: Oil rich in ALA caused similar immune modulation in cancer when compared with FO. 相似文献
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Benyam Kinde Harrison W. Gabel Caitlin S. Gilbert Eric C. Griffith Michael E. Greenberg 《Proceedings of the National Academy of Sciences of the United States of America》2015,112(22):6800-6806
DNA methylation at CpG dinucleotides is an important epigenetic regulator common to virtually all mammalian cell types, but recent evidence indicates that during early postnatal development neuronal genomes also accumulate uniquely high levels of two alternative forms of methylation, non-CpG methylation and hydroxymethylation. Here we discuss the distinct landscape of DNA methylation in neurons, how it is established, and how it might affect the binding and function of protein readers of DNA methylation. We review studies of one critical reader of DNA methylation in the brain, the Rett syndrome protein methyl CpG-binding protein 2 (MeCP2), and discuss how differential binding affinity of MeCP2 for non-CpG and hydroxymethylation may affect the function of this methyl-binding protein in the nervous system. 相似文献