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Bocker, M.T.; Hellwig, I.; Breiling, A.; Eckstein, V.; Ho, A.D.; Lyko, F. |
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Title |
Genome-wide promoter DNA methylation dynamics of human hematopoietic progenitor cells during differentiation and aging |
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Journal Article |
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Year |
2011 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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Volume |
117 |
Issue |
19 |
Pages |
e182-189 |
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Keywords |
Adult; Aging/*genetics; Cell Differentiation/*genetics; Cell Separation; DNA Methylation/*genetics; Flow Cytometry; Genome-Wide Association Study; Hematopoiesis/*genetics; Hematopoietic Stem Cells/*cytology; Humans; Oligonucleotide Array Sequence Analysis; Promoter Regions, Genetic/*genetics |
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Abstract |
DNA methylation plays an important role in the self-renewal of hematopoietic stem cells and in the commitment to the lymphoid or myeloid lineages. Using purified CD34 hematopoietic progenitor cells and differentiated myeloid cell populations from the same human samples, we obtained detailed methylation profiles at distinct stages of hematopoiesis. We identified a defined set of differentiation-related genes that are methylated in CD34 hematopoietic progenitor cells but show pronounced DNA hypomethylation in monocytes and in granulocytes. In addition, by comparing hematopoietic progenitor cells from umbilical cord blood to hematopoietic progenitor cells from peripheral blood of adult donors we were also able to analyze age-related methylation changes in CD34 cells. Interestingly, the methylation changes observed in older progenitor cells showed a bimodal pattern with hypomethylation of differentiation-associated genes and de novo methylation events resembling epigenetic mutations. Our results thus provide detailed insight into the methylation dynamics during differentiation and suggest that epigenetic changes contribute to hematopoietic progenitor cell aging. |
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ISSN |
1528-0020 |
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WP5 In vitro |
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PMID: 21427290 |
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Call Number |
UNIBAS @ david.schuermann @ Bocker2011 |
Serial |
71 |
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Author |
Boga, A.; Emre, M.; Sertdemir, Y.; Akillioglu, K.; Binokay, S.; Demirhan, O. |
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Title |
The effect of 900 and 1800MHz GSM-like radiofrequency irradiation and nicotine sulfate administration on the embryonic development of Xenopus laevis |
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Journal Article |
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Year |
2015 |
Publication |
Ecotoxicology and Environmental Safety |
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113 |
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May 2010 |
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378-390 |
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GSM-like radiofrequency radiation; Nicotine sulfate; Teratogenicity; Xenopus laevis; gsm-like radiofrequency radiation |
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Abstract |
The aim of this study was to investigate the effects of GSM-like radiofrequency electromagnetic radiation (RF EMR) and nicotine sulfate (NS) exposure on Xenopus embryonic development.The developmental effects of GSM-like RF-EMR (900–1800 MHz, at a SAR value of 1 W/kg and NS on Xenopus laevis embryos were investigated). Following the application of radiofrequency radiation and/or NS administration, the embryos were closely examined in order to determine their possible teratogenic effects. Xenopus frogs obtained from the Department of Physiology of the Cukurova University, in accordance described by the Standard Guide of the American Society for Testing and Materials (ASTM). Following the exposure of Xenopus embryos to RF-EMR at 900 and 1800 MHz (1.0 W/kg) for 4, 6 and 8 h; the whole body specific energy absorption rate (SAR) of the embryos was calculated. With the exception of irradiation at 1800 MHz no dramatic developmental anomalies were observed in the Xenopus embryos in association with RF-EMR applications. Combined RF-EMR and NS applications resulted in dramatic abnormalities and death among the Xenopus embryos. The study results indicated that GSM-like RF-EMR (e.g. radiation from cell phones) was not as harmful to Xenopus embryos as might have been expected. However, the combined effects of GSM-like RF-EMR and NS on Xenopus embryos were more severe than the effect of RF-EMR or NS alone. In conclusion, the study results appear to suggest that the combined use of nicotine and cell phones might result in more pronounced detrimental effects on the health of smokers. |
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Elsevier |
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WP5 In vitro; WP6 In vivo |
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UNIBAS @ david.schuermann @ |
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609 |
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Boorman, G.A.; Rafferty, C.N.; Ward, J.M.; Sills, R.C. |
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Title |
Leukemia and lymphoma incidence in rodents exposed to low-frequency magnetic fields |
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Journal Article |
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Year |
2000 |
Publication |
Radiation Research |
Abbreviated Journal |
Radiat Res |
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153 |
Issue |
5 Pt 2 |
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627-636 |
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Animals; Carcinogens; Cell Division/radiation effects; Cell Transformation, Neoplastic/radiation effects; Disease Models, Animal; Dose-Response Relationship, Radiation; Electromagnetic Fields/*adverse effects; Female; Humans; Leukemia/*etiology; Lymphoma/*etiology; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Rats; Rats, Inbred F344; Risk Assessment |
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A weak association between residential or occupational exposure to electric and magnetic fields (50/60 Hz fields) and an increased incidence of leukemia has been reported. Numerous animal studies have evaluated the potential association between magnetic-field exposure and leukemia. These include long-term (up to 2(1/2) years) bioassays, initiation/promotion studies, investigations in transgenic models, and tumor growth studies. Exposure to 60 Hz circularly polarized magnetic fields at 1,400 microT for 28 months did not affect lymphoma incidence in mice. The study included over 2000 C57BL/6J mice. In another study, 1000 B6C3F(1) mice exposed to 60 Hz magnetic fields up to 1000 microT for 2 years showed no increase in lymphomas. Approximately 400 transgenic Emu-Pim1 mice exposed to 50 Hz fields up to 1000 microT for up to 18 months had no increased incidence of leukemia. Similarly, Trp53(+/-) mice and Pim1transgenic mice exposed to 60 Hz magnetic fields for 23 weeks showed no increased incidence of lymphoma. Three studies in F344 rats exposed to 50 or 60 Hz magnetic fields up to 5 mT showed no increased incidence of leukemia. The combined animal bioassay results are nearly uniformly negative for magnetic-field exposures enhancing leukemia and weaken the possible epidemiological association between magnetic-field exposures and leukemia in humans as suggested by epidemiological data. |
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National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA |
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English |
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0033-7587 |
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WP6 In vivo |
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PMID:10790285 |
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ITEM @ geertje.lewin @ |
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140 |
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Borst, L.; Wesolowska, A.; Joshi, T.; Borup, R.; Nielsen, F.C.; Andersen, M.K.; Jonsson, O.G.; Wehner, P.S.; Wesenberg, F.; Frost, B.M.; Gupta, R.; Schmiegelow, K. |
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Title |
Genome-wide analysis of cytogenetic aberrations in ETV6/RUNX1-positive childhood acute lymphoblastic leukaemia |
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Journal Article |
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Year |
2012 |
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British Journal of Haematology |
Abbreviated Journal |
Br J Haematol |
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The chromosomal translocation t(12;21) resulting in the ETV6/RUNX1 fusion gene is the most frequent structural cytogenetic abnormality among patients with childhood acute lymphoblastic leukaemia (ALL). We investigated 62 ETV6/RUNX1-positive childhood ALL patients by single nucleotide polymorphism array to explore acquired copy number alterations (CNAs) at diagnosis. The mean number of CNAs was 2.82 (range 0-14). Concordance with available G-band karyotyping and comparative genomic hybridization was 93%. Based on three major protein-protein complexes disrupted by these CNAs, patients could be categorized into four distinct subgroups, defined by different underlying biological mechanisms relevant to the aetiology of childhood ALL. When recurrent CNAs were evaluated by an oncogenetic tree analysis classifying their sequential order, the most common genetic aberrations (deletions of 6q, 9p, 13q and X, and gains of 10 and 21) seemed independent of each other. Finally, we identified the most common regions with recurrent gains and losses, which comprise microRNA clusters with known oncogenic or tumour-suppressive roles. The present study sheds further light on the genetic diversity of ETV6/RUNX1-positive childhood ALL, which may be important for understanding poor responses among this otherwise highly curable subset of ALL and lead to novel targeted treatment strategies. |
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Clinic for Paediatric and Adolescent Medicine, The Juliane Marie Centre, The University Hospital Rigshospitalet, Copenhagen |
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0007-1048 |
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WP6 In vivo |
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PMID:22404039 |
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CBM.UAM @ ccobaleda @ |
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167 |
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Author |
Brisdelli, F.; Bennato, F.; Bozzi, A.; Cinque, B.; Mancini, F.; Iorio, R. |
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Title |
ELF-MF attenuates quercetin-induced apoptosis in K562 cells through modulating the expression of Bcl-2 family proteins |
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Newspaper Article |
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2014 |
Publication |
Molecular and Cellular Biochemistry |
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33-43 |
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Apoptosis; Bcl-2; Elf-Mf; K562 cells; Quercetin |
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Abstract |
This study investigated the effects of sinusoidal ELF-MF (1 mT; 50 Hz) on the apoptosis induced by four different compounds, namely vinblastine, etoposide, quercetin, and resveratrol, in human K562 chronic myeloid leukemia cells. The exposure to ELF-MF did not affect growth and viability of untreated K562 cells and did not influence the anti-proliferative effects of resveratrol, vinblastine, and etoposide. On the contrary, in quercetin-treated cells, exposure to ELF-MF significantly reduced the percentage of apoptotic cells and the caspase-3 activity and modified the cell cycle profile especially after 48 h of exposure. In addition, the simultaneous treatments for 24 h with quercetin plus ELF-MF increased Bcl-2 protein expression and prevented quercetin-induced downregulation of Mcl-1 and Bcl-xL. Finally, an increase of HSP70 expression was also observed after prolonged ELF-MF treatment. The ELF-MF-dependent modulation of the expression of anti-apoptotic Bcl-2 family and Hsp70 proteins could act as a pro-survival mechanism in K562 cells. |
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UNIBAS @ david.schuermann @ |
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572 |
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