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Chair(s): Paretzke, Herwig
(SY058) RISC RAD workpackage 3: pre-neoplastic lesions and tumour development.
Bouffler, Simon*,1, 1 Radiation Protection Division, Chilton, Oxfordshire, UK
ABSTRACT- The aim of workpackage (WP) 3 is to provide a more complete description of the temporal sequence of genetic and epigenetic events which drive radiation tumorigenesis in animal models of skin, intestinal, bone, lung, mammary and haemopoietic radiogenic cancers. These tumour models cover the major contributions to excess radiation cancer risk defined in epidemiological studies. A supplementary aim is to gain quantitative data on the influence of dose protraction, age-at-irradiation, and gender on radiation carcinogenesis. A central theme is the analysis of early pre-cancerous lesions as well as end-stage tumours. The data generated can then be used to develop, with WP 5, system-specific biologically based models of radiation cancer risk. These approaches will contribute to the development of more generalised cancer risk projection models based on sound knowledge of the biology of radiation carcinogenesis. This approach makes no specific assumptions of the nature of the mechanisms acting - involvements of non-targeted phenomena such as genomic instability and possibly bystander effects will be apparent. Many key elements of the work programme are underway including: quantitative studies of skin carcinogenesis and myeloid leukaemogenesis, development of transcriptome analysis tools, development of tools for analysis of methylation status, identification and collection of early lesions in bone, skin and intestine and quantitative analysis of critical target gene losses at early stages of AML development. Over the remainder of the project the analytical tools will be refined and applied, information on early stage gene losses will be obtained. This detailed information will be critical to determine the action of radiation cancer risk modifier genes (the topic of WP 4) as well as developmental and environmental influences on radiation carcinogenesis. Taken together the information will provide a more complete picture of the routes by which radiation changes normal cells into malignant tumours.
Key words: carcinogenesis, riscrad, low-dose
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