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Idoia Martin‐Guerrero Birgit Burkhardt Markus Kreuz Thorsten Zenz Ilske Oschlies Norbert Arnold Michael Baudis Susanne Bens Africa García‐Orad Jasmin Lisfeld Carsten Schwaenen Monika Szczepanowski Swen Wessendorf Michael Pfreundschuh Lorenz Trümper Wolfram Klapper Reiner Siebert 《Genes, chromosomes & cancer》2013,52(2):150-155
Translocations affecting chromosome subband 6p25.3 containing the IRF4 gene have been recently described as characteristic alterations in a molecularly distinct subset of germinal center B‐cell‐derived lymphomas. Secondary changes have yet only been described in few of these lymphomas. Here, we performed array‐comparative genomic hybridization and molecular inversion probe microarray analyses on DNA from 12 formalin‐fixed paraffin‐embedded and two fresh‐frozen IRF4 translocation‐positive lymphomas, which together with the previously published data on nine cases allowed the extension of copy number analyses to a total of 23 of these lymphomas. All except one case carried chromosomal imbalances, most frequently gains in Xq28, 11q22.3‐qter, and 7q32.1‐qter and losses in 6q13‐16.1, 15q14‐22.31, and 17p. No recurrent copy‐neutral losses of heterozygosity were observed. TP53 point mutations were detected in three of six cases with loss of 17p. Overall this study unravels a recurrent pattern of secondary genetic alterations in IRF4 translocation‐positive lymphomas. © 2012 Wiley Periodicals, Inc. 相似文献
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RHAMM, a receptor for hyaluronan-mediated motility, compensates for CD44 in inflamed CD44-knockout mice: a different interpretation of redundancy 下载免费PDF全文
Nedvetzki S Gonen E Assayag N Reich R Williams RO Thurmond RL Huang JF Neudecker BA Wang FS Wang FS Turley EA Naor D 《Proceedings of the National Academy of Sciences of the United States of America》2004,101(52):18081-18086
We report here that joint inflammation in collagen-induced arthritis is more aggravated in CD44-knockout mice than in WT mice, and we provide evidence for molecular redundancy as a causal factor. Furthermore, we show that under the inflammatory cascade, RHAMM (receptor for hyaluronan-mediated motility), a hyaluronan receptor distinct from CD44, compensates for the loss of CD44 in binding hyaluronic acid, supporting cell migration, up-regulating genes involved with inflammation (as assessed by microarrays containing 13,000 cDNA clones), and exacerbating collagen-induced arthritis. Interestingly, we further found that the compensation for loss of the CD44 gene does not occur because of enhanced expression of the redundant gene (RHAMM), but rather because the loss of CD44 allows increased accumulation of the hyaluronic acid substrate, with which both CD44 and RHAMM engage, thus enabling augmented signaling through RHAMM. This model enlightens several aspects of molecular redundancy, which is widely discussed in many scientific circles, but the processes are still ill defined. 相似文献
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Assmus B Urbich C Aicher A Hofmann WK Haendeler J Rössig L Spyridopoulos I Zeiher AM Dimmeler S 《Circulation research》2003,92(9):1049-1055
Endothelial progenitor cells (EPCs) play an important role in postnatal neovascularization of ischemic tissue. Ex vivo expansion of EPCs might be useful for potential clinical cell therapy of myocardial ischemia. However, cultivation of primary cells leads to cellular aging (senescence), thereby severely limiting the proliferative capacity. Therefore, we investigated whether statins might be able to prevent senescence of EPCs. EPCs were isolated from peripheral blood and characterized. After ex vivo cultivation, EPCs became senescent as determined by acidic beta-galactosidase staining. Atorvastatin or mevastatin dose-dependently inhibited the onset of EPC senescence in culture. Moreover, atorvastatin increased proliferation of EPCs as assessed by BrdU incorporation and colony-forming capacity. Whereas geranylgeranylpyrophosphate or farnesylpyrophosphate reduced the senescence inhibitory effect of atorvastatin, NO synthase inhibition, antioxidants, or Rho kinase inhibitors had no effect. To get further insights into the underlying downstream effects of statins, we measured telomerase activity and determined the expression of various cell cycle regulatory genes by using a microarray assay. Whereas telomerase activity did not change, atorvastatin modulated expression of cell cycle genes including upregulation of cyclins and downregulation of the cell cycle inhibitor p27Kip1. Taken together, statins inhibited senescence of EPCs independent of NO, reactive oxygen species, and Rho kinase, but dependent on geranylgeranylpyrophosphate. Atorvastatin-mediated prevention of EPC senescence appears to be mediated by the regulation of various cell cycle proteins. The inhibition of EPC senescence and induction of EPC proliferation by statins in vitro may importantly improve the functional activity of EPCs for potential cell therapy. 相似文献
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Krone N Reisch N Idkowiak J Dhir V Ivison HE Hughes BA Rose IT O'Neil DM Vijzelaar R Smith MJ MacDonald F Cole TR Adolphs N Barton JS Blair EM Braddock SR Collins F Cragun DL Dattani MT Day R Dougan S Feist M Gottschalk ME Gregory JW Haim M Harrison R Olney AH Hauffa BP Hindmarsh PC Hopkin RJ Jira PE Kempers M Kerstens MN Khalifa MM Köhler B Maiter D Nielsen S O'Riordan SM Roth CL Shane KP Silink M Stikkelbroeck NM Sweeney E Szarras-Czapnik M Waterson JR Williamson L Hartmann MF Taylor NF 《The Journal of clinical endocrinology and metabolism》2012,97(2):E257-E267