Genomic instability and radiation-induced cancer (RADINSTAB), Final report (summary)
Project ID: FIGH-CT-1999-00003Funded under: FP5-EAECTP C
The discovery of radiation-induced genomic instability has raised concern for its implication in the radiation protection of the public, especially quantification of human risk at low doses and high LET exposure. The main source of information on radiation-induced human cancer risk comes from epidemiological data of exposed populations. However, direct information is available only at relatively large doses, and mostly for low-LET X- and gamma-rays. A linear extrapolation from these data is applied at lower doses, which are more relevant in terms of exposure of general population and radiation workers. Additional extrapolation is applied to other radiation types. The shape of the cancer dose-response curve at low doses is a matter of constant debate; arguments are ranging from threshold (or even hormesis) to non-threshold supralinear responses. Biological modelling of radiation carcinogenesis may offer a tool to study the risk in the low-dose region. Non-targeted radiation effects, such as genomic instability (novel mutations and cell death in the progeny of irradiated cells) and bystander effects (effects observed in the neighbouring cells not directly impacted by radiation), may be important early steps in the development of radiation-induced cancer. Understanding of underlying mechanisms may have profound consequences on cancer risk assessment.
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Record Number: 8930 / Last updated on: 2008-01-24