Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2112833 | Cancer Letters | 2013 | 10 Pages |
•Low dose hyper-radiosensitivity has been demonstrated in 75% of the 50 mammalian normal and malignant cells tested to date.•Low dose hyper-radiosensitivity is induced by a variety of radiation qualities.•Low dose hyper-radiosensitivity is associated with defective double strand breaks DNA repair pathways.•The clinical relevance of Low dose hyper-radiosensitivity in radiation oncology is a matter of debate.
This review article provides a comprehensive overview of the experimental data detailing the incidence, mechanism and significance of low dose hyper-radiosensitivity (HRS). Important discoveries gained from past and present studies are mapped and highlighted to illustrate the pathway to our current understanding of HRS and the impact of HRS on the cellular response to radiation in mammalian cells. Particular attention is paid to the balance of evidence suggesting a role for DNA repair processes in the response, evidence suggesting a role for the cell cycle checkpoint processes, and evidence investigating the clinical implications/relevance of the effect.