In vivo formation of gamma-H2AX and 53BP1 DNA repair foci in blood cells after radioiodine therapy of differentiated thyroid cancer.

@article{Lassmann2010InVF,
  title={In vivo formation of gamma-H2AX and 53BP1 DNA repair foci in blood cells after radioiodine therapy of differentiated thyroid cancer.},
  author={Michael Lassmann and Heribert Haenscheid and Daniela Gassen and Johannes Biko and Viktor Meineke and Christoph Reiners and Harry Scherthan},
  journal={Journal of nuclear medicine : official publication, Society of Nuclear Medicine},
  year={2010},
  volume={51 8},
  pages={
          1318-25
        }
}
UNLABELLED DNA double-strand breaks (DSBs) are critical cellular lesions that can result from ionizing radiation exposure. A marker for DSB formation is the phosphorylated form of the histone H2 variant H2AX (gamma-H2AX). DSBs also attract the damage sensor p53-binding protein 1 (53BP1) to the DSB-containing chromatin, because 53BP1 associates with the DSB-surrounding chromatin. We studied the induction, persistence, and disappearance of radiation-induced gamma-H2AX and 53BP1 foci after the… CONTINUE READING
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