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Residual 53BP/γ-H2AX Foci in Human Lymphocytes

Long time persistence of residual 53BP1/γ-H2AX foci in human lymphocytes in relationship to apoptosis, chromatin condensation and biological dosimetry

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Pages 736-745 | Received 13 Aug 2010, Accepted 16 Mar 2011, Published online: 01 Jul 2011

References

  • Belyaev IY. 2010. Radiation-induced DNA repair foci: Spatio-temporal aspects of formation, application for assessment of radiosensitivity and biological dosimetry. Mutation Research 704:132–141.
  • Belyaev IY, Alipov YD, Matronchik AY. 1998. Cell density dependent response of E. coli cells to weak ELF magnetic fields. Bioelectromagnetics 19:300–309.
  • Belyaev IY, Czene S, Harms-Ringdahl M. 2001. Changes in chromatin conformation during radiation-induced apoptosis in human lymphocytes. Radiation Research 156:355–364.
  • Belyaev IY, Eriksson S, Nygren J, Torudd J, Harms-Ringdahl M. 1999. Effects of ethidium bromide on DNA loop organisation in human lymphocytes measured by anomalous viscosity time dependence and single cell gel electrophoresis. Biochim Biophys Acta 1428:348–356.
  • Bhogal N, Kaspler P, Jalali F, Hyrien O, Chen R, Hill RP, Bristow RG. 2010. Late residual gamma-H2AX foci in murine skin are dose responsive and predict radiosensitivity in vivo. Radiation Research 173:1–9.
  • Dikomey E, Borgmann K, Peacock J, Jung H. 2003. Why recent studies relating normal tissue response to individual radiosensitivity might have failed and how new studies should be performed. International Journal of Radiation Oncology, Biology, Physics 56:1194–1200.
  • Fernandez-Capetillo O, Chen HT, Celeste A, Ward I, Romanienko PJ, Morales JC, Naka K, Xia Z, Camerini-Otero RD, Motoyama N, Carpenter PB, Bonner WM, Chen J, Nussenzweig A. 2002. DNA damage-induced G2-M checkpoint activation by histone H2AX and 53BP1. Nature Cell Biology 4:993–997.
  • Huang X, Halicka HD, Traganos F, Tanaka T, Kurose A, Darzynkiewicz Z. 2005. Cytometric assessment of DNA damage in relation to cell cycle phase and apoptosis. Cell Proliferation 38:223–243.
  • Huang X, Okafuji M, Traganos F, Luther E, Holden E, Darzynkiewicz Z. 2004. Assessment of histone H2AX phosphorylation induced by DNA topoisomerase I and II inhibitors topotecan and mitoxantrone and by the DNA cross-linking agent cisplatin. Cytometry 58A:99–110.
  • Chebel A, Bauwens S, Gerland LM, Belleville A, Urbanowicz I, de Climens AR, Tourneur Y, Chien WW, Catallo R, Salles G, Gilson E, Ffrench M. 2009. Telomere uncapping during in vitro T-lymphocyte senescence. Aging Cell 8:52–64.
  • Iwabuchi K, Basu BP, Kysela B, Kurihara T, Shibata M, Guan D, Cao Y, Hamada T, Imamura K, Jeggo PA, Date T, Doherty AJ. 2003. Potential role for 53BP1 in DNA end-joining repair through direct interaction with DNA. Journal of Biological Chemistry 278:36487–36495.
  • Joubert A, Zimmerman KM, Bencokova Z, Gastaldo J, Chavaudra N, Favaudon V, Arlett CF, Foray N. 2008. DNA double-strand break repair defects in syndromes associated with acute radiation response: At least two different assays to predict intrinsic radiosensitivity? International Journal of Radiation Biology 84:107–125.
  • Kao GD, McKenna WG, Guenther MG, Muschel RJ, Lazar MA, Yen TJ. 2003. Histone deacetylase 4 interacts with 53BP1 to mediate the DNA damage response. Journal of Cell Biology 160:1017–1027.
  • Kuhne M, Riballo E, Rief N, Rothkamm K, Jeggo PA, Löbrich M. 2004. A double-strand break repair defect in ATM-deficient cells contributes to radiosensitivity. Cancer Research 64:500–508.
  • Löbrich M, Rief N, Kuhne M, Heckmann M, Fleckenstein J, Rube C, Uder M. 2005. In vivo formation and repair of DNA double-strand breaks after computed tomography examinations. Proceedings of the National Academy of Sciences of the USA 102:8984–8989.
  • MacPhail SH, Banath JP, Yu TY, Chu EH, Lambur H, Olive PL. 2003a. Expression of phosphorylated histone H2AX in cultured cell lines following exposure to X-rays. International Journal of Radiation Biology 79:351–358.
  • MacPhail SH, Banath JP, Yu Y, Chu E, Olive PL. 2003b. Cell cycle-dependent expression of phosphorylated histone H2AX: Reduced expression in unirradiated but not X-irradiated G1-phase cells. Radiation Research 159:759–767.
  • Markova E, Schultz N, Belyaev IY. 2007. Kinetics and dose-response of residual 53BP1/gamma-H2AX foci: Co-localization, relationship with DSB repair and clonogenic survival. International Journal of Radiation Biology 83:319–329.
  • Marti TM, Hefner E, Feeney L, Natale V, Cleaver JE. 2006. H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks. Proceedings of the National Academy of Sciences of the USA 103:9891–9896.
  • Meijer AE, Kronqvist US, Lewensohn R, Harms-Ringdahl M. 1998. RBE for the induction of apoptosis in human peripheral lymphocytes exposed in vitro to high-LET radiation generated by accelerated nitrogen ions. International Journal of Radiation Biology 73:169–177.
  • Mognato M, Girardi C, Fabris S, Celotti L. 2009. DNA repair in modeled microgravity: Double strand break rejoining activity in human lymphocytes irradiated with gamma-rays. Mutation Research 663:32–39.
  • Nowak E, Etienne O, Millet P, Lages CS, Mathieu C, Mouthon MA, Boussin FD. 2006. Radiation-induced H2AX phosphorylation and neural precursor apoptosis in the developing brain of mice. Radiation Research 165:155–164.
  • Olive PL, Banath JP. 2004. Phosphorylation of histone H2AX as a measure of radiosensitivity. International Journal of Radiation Oncology Biology Physics 58:331–335.
  • Olive PL, Banath JP, Keyes M. 2008. Residual gamma-H2AX after irradiation of human lymphocytes and monocytes in vitro and its relation to late effects after prostate brachytherapy. Radiotherapy & Oncology 86:336–346.
  • Prasanna PG, Hamel CJ, Escalada ND, Duffy KL, Blakely WF. 2002. Biological dosimetry using human interphase peripheral blood lymphocytes. Military medicine 167:10–12.
  • Rappold I, Iwabuchi K, Date T, Chen J. 2001. Tumor suppressor p53 binding protein 1 (53BP1) is involved in DNA damage-signaling pathways. Journal of Cell Biology 153: 613–620.
  • Redon CE, Dickey JS, Bonner WM, Sedelnikova OA. 2009. [gamma]-H2AX as a biomarker of DNA damage induced by ionizing radiation in human peripheral blood lymphocytes and artificial skin. Advances in Space Research 43:1171–1178.
  • Redon CE, Nakamura AJ, Gouliaeva K, Rahman A, Blakely WF, Bonner WM. 2010. The use of gamma-H2AX as a biodosimeter for total-body radiation exposure in non-human primates. PLoS One 5:e15544.
  • Rodier F, Munoz DP, Teachenor R, Chu V, Le O, Bhaumik D, Coppe JP, Campeau E, Beausejour CM, Kim SH, Davalos AR, Campisi J. 2010. DNA-SCARS: Distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion. Journal of Cell Science 124:68–81.
  • Rogakou EP, Boon C, Redon C, Bonner WM. 1999. Megabase chromatin domains involved in DNA double-strand breaks in vivo. Journal of Cell Biology 146:905–916.
  • Rothkamm K, Balroop S, Shekhdar J, Fernie P, Goh V. 2007. Leukocyte DNA damage after multi-detector row CT: A quantitative biomarker of low-level radiation exposure. Radiology 242:244–251.
  • Rothkamm K, Löbrich M. 2003. Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses. Proceedings of the National Academy of Science of the USA 100:5057–5062.
  • Sak A, Grehl S, Erichsen P, Engelhard M, Grannass A, Levegrun S, Pottgen C, Groneberg M, Stuschke M. 2007. gamma-H2AX foci formation in peripheral blood lymphocytes of tumor patients after local radiotherapy to different sites of the body: Dependence on the dose-distribution, irradiated site and time from start of treatment. International Journal of Radiation Biology 83:639–652.
  • Sak A, Stueben G, Groneberg M, Bocker W, Stuschke M. 2005. Targeting of Rad51-dependent homologous recombination: Implications for the radiation sensitivity of human lung cancer cell lines. British Journal of Cancer 92:1089–1097.
  • Sedelnikova OA, Horikawa I, Redon C, Nakamura A, Zimonjic DB, Popescu NC, Bonner WM. 2008. Delayed kinetics of DNA double-strand break processing in normal and pathological aging. Aging Cell 7:89–100.
  • Sedelnikova OA, Rogakou EP, Panyutin IG, Bonner WM. 2002. Quantitative detection of (125)IdU-induced DNA double-strand breaks with gamma-H2AX antibody. Radiation Research 158:486–492.
  • Short SC, Martindale C, Bourne S, Brand G, Woodcock M, Johnston P. 2007. DNA repair after irradiation in glioma cells and normal human astrocytes. Neuro-Oncology 9:404–411.
  • Scherthan H, Hieber L, Braselmann H, Meineke V, Zitzelsberger H. 2008. Accumulation of DSBs in gamma-H2AX domains fuel chromosomal aberrations. Biochemical and Biophysical Research Communications 371:694–697.
  • Schultz LB, Chehab NH, Malikzay A, Halazonetis TD. 2000. p53 binding protein 1 (53BP1) is an early participant in the cellular response to DNA double-strand breaks. Journal of Cell Biology 151:1381–1390.
  • Suzuki M, Suzuki K, Kodama S, Watanabe M. 2006. Phosphorylated histone H2AX foci persist on rejoined mitotic chromosomes in normal human diploid cells exposed to ionizing radiation. Radiation Research 165:269–276.
  • Taneja N, Davis M, Choy JS, Beckett MA, Singh R, Kron SJ, Weichselbaum RR. 2004. Histone H2AX phosphorylation as a predictor of radiosensitivity and target for radiotherapy. Journal of Biological Chemistry 279:2273–2280.
  • Torudd J, Protopopova M, Sarimov R, Nygren J, Eriksson S, Markova E, Chovanec M, Selivanova G, Belyaev IY. 2005. Dose-response for radiation-induced apoptosis, residual 53BP1 foci and DNA-loop relaxation in human lymphocytes. International Journal of Radiation Biology 81:125–138.
  • Vilasova Z, Rezacova M, Vavrova J, Tichy A, Vokurkova D, Zoelzer F, Rehakova Z, Osterreicher J, Lukasova E. 2008. Changes in phosphorylation of histone H2A.X and p53 in response of peripheral blood lymphocytes to gamma irradiation. Acta biochimica Polonica 55:381–390.
  • Yamauchi M, Oka Y, Yamamoto M, Niimura K, Uchida M, Kodama S, Watanabe M, Sekine I, Yamashita S, Suzuki K. 2008. Growth of persistent foci of DNA damage checkpoint factors is essential for amplification of G1 checkpoint signaling. DNA Repair (Amst) 7:405–417.

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