| pubmed-article:20660387 | pubmed:abstractText | 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 first (131)I therapy of patients with differentiated thyroid carcinoma, a model for protracted, continuous, internal whole-body irradiation. | lld:pubmed |
