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Author |
Chatterton, Z.; Morenos, L.; Mechinaud, F.; Ashley, D.M.; Craig, J.M.; Sexton-Oates, A.; Halemba, M.S.; Parkinson-Bates, M.; Ng, J.; Morrison, D.; Carroll, W.L.; Saffery, R.; Wong, N.C. |
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Title |
Epigenetic deregulation in pediatric acute lymphoblastic leukemia |
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Journal Article |
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Year  |
2014 |
Publication |
Epigenetics : Official Journal of the DNA Methylation Society |
Abbreviated Journal |
Epigenetics |
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Volume |
9 |
Issue |
3 |
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Keywords |
All; B-cell; DNA methylation; acute lymphoblastic leukemia; epigenetics; hematology; leukemia |
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Abstract |
Similar to most cancers, genome-wide DNA methylation profiles are commonly altered in pediatric acute lymphoblastic leukemia (ALL); however, recent observations highlight that a large portion of malignancy-associated DNA methylation alterations are not accompanied by related gene expression changes. By analyzing and integrating the methylome and transcriptome profiles of pediatric B-cell ALL cases and primary tissue controls, we report 325 genes hypermethylated and downregulated and 45 genes hypomethylated and upregulated in pediatric B-cell ALL, irrespective of subtype. Repressed cation channel subunits and cAMP signaling activators and transducers are overrepresented, potentially indicating a reduced cellular potential to receive and propagate apoptotic signals. Furthermore, we report specific DNA methylation alterations with concurrent gene expression changes within individual ALL subtypes. The ETV6-RUNX1 translocation was associated with downregulation of ASNS and upregulation of the EPO-receptor, while Hyperdiploid patients (> 50 chr) displayed upregulation of B-cell lymphoma (BCL) members and repression of PTPRG and FHIT. In combination, these data indicate genetically distinct B-cell ALL subtypes contain cooperative epimutations and genome-wide epigenetic deregulation is common across all B-cell ALL subtypes. |
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Address |
Murdoch Childrens Research Institute; The University of Melbourne Department of Paediatrics at the Royal Children's Hospital; Victoria, VIC Australia |
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ISSN |
1559-2294 |
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Notes |
PMID:24394348 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
459 |
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Author |
Lento, W.; Ito, T.; Zhao, C.; Harris, J.R.; Huang, W.; Jiang, C.; Owzar, K.; Piryani, S.; Racioppi, L.; Chao, N.; Reya, T. |
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Title |
Loss of beta-catenin triggers oxidative stress and impairs hematopoietic regeneration |
Type |
Journal Article |
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Year |
2014 |
Publication |
Genes & Development |
Abbreviated Journal |
Genes Dev |
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Volume |
28 |
Issue |
9 |
Pages |
995-1004 |
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Keywords |
Wnt signaling; hematopoietic stem cells; oxidative stress; regeneration; β-catenin |
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Abstract |
Accidental or deliberate ionizing radiation exposure can be fatal due to widespread hematopoietic destruction. However, little is known about either the course of injury or the molecular pathways that regulate the subsequent regenerative response. Here we show that the Wnt signaling pathway is critically important for regeneration after radiation-induced injury. Using Wnt reporter mice, we show that radiation triggers activation of Wnt signaling in hematopoietic stem and progenitor cells. beta-Catenin-deficient mice, which lack the ability to activate canonical Wnt signaling, exhibited impaired hematopoietic stem cell regeneration and bone marrow recovery after radiation. We found that, as part of the mechanism, hematopoietic stem cells lacking beta-catenin fail to suppress the generation of reactive oxygen species and cannot resolve DNA double-strand breaks after radiation. Consistent with the impaired response to radiation, beta-catenin-deficient mice are also unable to recover effectively after chemotherapy. Collectively, these data indicate that regenerative responses to distinct hematopoietic injuries share a genetic dependence on beta-catenin and raise the possibility that modulation of Wnt signaling may be a path to improving bone marrow recovery after damage. |
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Department of Pharmacology, University of California at San Diego School of Medicine, La Jolla, California 92093, USA |
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0890-9369 |
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PMID:24788518 |
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CBM.UAM @ ccobaleda @ |
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461 |
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Engels, S.; Schneider, N.-L.; Lefeldt, N.; Hein, C.M.; Zapka, M.; Michalik, A.; Elbers, D.; Kittel, A.; Hore, P.J.; Mouritsen, H. |
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Title |
Anthropogenic electromagnetic noise disrupts magnetic compass orientation in a migratory bird |
Type |
Journal Article |
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Year |
2014 |
Publication |
Nature |
Abbreviated Journal |
Nature |
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Electromagnetic noise is emitted everywhere humans use electronic devices. For decades, it has been hotly debated whether man-made electric and magnetic fields affect biological processes, including human health. So far, no putative effect of anthropogenic electromagnetic noise at intensities below the guidelines adopted by the World Health Organization has withstood the test of independent replication under truly blinded experimental conditions. No effect has therefore been widely accepted as scientifically proven. Here we show that migratory birds are unable to use their magnetic compass in the presence of urban electromagnetic noise. When European robins, Erithacus rubecula, were exposed to the background electromagnetic noise present in unscreened wooden huts at the University of Oldenburg campus, they could not orient using their magnetic compass. Their magnetic orientation capabilities reappeared in electrically grounded, aluminium-screened huts, which attenuated electromagnetic noise in the frequency range from 50 kHz to 5 MHz by approximately two orders of magnitude. When the grounding was removed or when broadband electromagnetic noise was deliberately generated inside the screened and grounded huts, the birds again lost their magnetic orientation capabilities. The disruptive effect of radiofrequency electromagnetic fields is not confined to a narrow frequency band and birds tested far from sources of electromagnetic noise required no screening to orient with their magnetic compass. These fully double-blinded tests document a reproducible effect of anthropogenic electromagnetic noise on the behaviour of an intact vertebrate. |
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1] Institut fur Biologie und Umweltwissenschaften, Universitat Oldenburg, D-26111 Oldenburg, Germany [2] Research Centre for Neurosensory Sciences, University of Oldenburg, D-26111 Oldenburg, Germany |
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0028-0836 |
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Notes |
PMID:24805233 |
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CBM.UAM @ ccobaleda @ |
Serial |
462 |
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Author |
Kirschvink, J.L. |
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Title |
Sensory biology: Radio waves zap the biomagnetic compass |
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Journal Article |
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Year |
2014 |
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Nature |
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Nature |
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Division of Geological and Planetary Sciences, California Institute of Technology, Pasadena, California 91125, USA, and at the Earth-Life Science Institute, Tokyo Institute of Technology, Japan |
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0028-0836 |
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Notes |
PMID:24805230 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
463 |
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Author |
Guerra, P.A.; Gegear, R.J.; Reppert, S.M. |
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Title |
A magnetic compass aids monarch butterfly migration |
Type |
Journal Article |
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Year |
2014 |
Publication |
Nature Communications |
Abbreviated Journal |
Nat Commun |
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Volume |
5 |
Issue |
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Pages |
4164 |
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Abstract |
Convincing evidence that migrant monarch butterflies (Danaus plexippus) use a magnetic compass to aid their fall migration has been lacking from the spectacular navigational capabilities of this species. Here we use flight simulator studies to show that migrants indeed possess an inclination magnetic compass to help direct their flight equatorward in the fall. The use of this inclination compass is light-dependent utilizing ultraviolet-A/blue light between 380 and 420 nm. Notably, the significance of light <420 nm for inclination compass function was not considered in previous monarch studies. The antennae are important for the inclination compass because they appear to contain light-sensitive magnetosensors. For migratory monarchs, the inclination compass may serve as an important orientation mechanism when directional daylight cues are unavailable and may also augment time-compensated sun compass orientation for appropriate directionality throughout the migration. |
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Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, Massachusetts 01605, USA |
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ISSN |
2041-1723 |
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Notes |
PMID:24960099 |
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CBM.UAM @ ccobaleda @ |
Serial |
533 |
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