The aim of biological dosimetry is to estimate the dose and the associated uncertainty to which an accident victim was exposed. This process requires the use of the maximum-likelihood method for fitting a calibration curve, a procedure that is not implemented in most statistical computer programs. Several laboratories have produced their own programs, but these are frequently not user-friendly and not available to outside users. We developed a software for fitting a linear-quadratic dose-response relationship by the method of maximum-likelihood and for estimating a dose from the number of aberrations observed. The program called as CABAS consists of the main curve-fitting and dose estimating module and modules for calculating the dose in cases of partial body exposure, for estimating the minimum number of cells necessary to detect a given dose of radiation and for calculating the dose in the case of a protracted exposure. The program is freely available at http://www.pu.kielce.pl/ibiol/cabas.

This paper reviews cytogenetic methods of biological dosimetry. The most reliable indicator of exposure to ionizing radiation is the observation of dicentrics in human peripheral lymphocytes. The major disadvantage is that dicentrics cannot be used for exposures that occur many years prior to blood sampling. In such cases, translocations are the aberrations of choice, and recent developments in their measurement using fluorescence in situ hybridization techniques are highlighted.

The sensitivity of ApcMin/+ mice to the induction of intestinal tumours by radiation was shown to be in the order: 10 d neonates>2 d neonates>35 d young adults>14 d fetus>7 d embryo.

The mapping of genes which affect individual cancer risk is an important but complex challenge. A surrogate assay of susceptibility to radiation-induced acute myeloid leukaemia (AML) in the mouse based on chromosomal radiosensitivity has been developed and validated. This assay was applied to the mapping of radiation-induced AML risk modifier loci by association with microsatellite markers. A region on chromosome (chr) 18 with strong association is identified and confirmed by backcross analysis. Additional loci on chrs 8 and 13 show significant association. A key candidate gene Rbbp8 on chr18 is identified. Rbbp8 is shown to be upregulated in response to X-irradiation in the AML sensitive CBA strain but not AML resistant C57BL/6 strain. This study demonstrates the strength of utilizing surrogate endpoints of cancer susceptibility in the mapping of mouse loci and identifies additional loci that may affect radiation cancer risk.

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