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Schmid, T.E.* ; Zlobinskaya, O.* ; Multhoff, G.

Differences in phosphorylated histone H2AX foci formation and removal of cells exposed to low and high linear energy transfer radiation.

Curr. Genomics 13, 418-425 (2012)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The use of particle ion beams in cancer radiotherapy has a long history. Today, beams of protons or heavy ions, predominantly carbon ions, can be accelerated to precisely calculated energies which can be accurately targeted to tumors. This particle therapy works by damaging the DNA of tissue cells, ultimately causing their death. Among the different types of DNA lesions, the formation of DNA double strand breaks is considered to be the most relevant of deleterious damages of ionizing radiation in cells. It is well-known that the extremely large localized energy deposition can lead to complex types of DNA double strand breaks. These effects can lead to cell death, mutations, genomic instability, or carcinogenesis. Complex double strand breaks can increase the probability of mis-rejoining by NHEJ. As a consequence differences in the repair kinetics following high and low LET irradiation qualities are attributed mainly to quantitative differences in their contributions of the fast and slow repair component. In general, there is a higher contribution of the slow component of DNA double strand repair after exposure to high LET radiation, which is thought to reflect the increased amount of complex DNA double strand breaks. These can be accurately measured by the γ-H2AX assay, because the number of phosphorylated H2AX foci correlates well with the number of double strand breaks induced by low or / and high LET radiation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter DNA double strand breaks; linear energy transfer; radiation; gamma-H2AX foci
ISSN (print) / ISBN 1389-2029
e-ISSN 1875-5488
Zeitschrift Current Genomics
Quellenangaben Band: 13, Heft: 6, Seiten: 418-425 Artikelnummer: , Supplement: ,
Verlag Bentham Science Publishers
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Innate Immunity in Tumor Biology (IBMI-KTB)