Ionizing radiation sole cause of chronic myelogenous leukemia. The mechanism by which this occurs is well understood, but quantitative models predicting the level of risk remain controversial. The most widely accepted model posits that the incidence of cancers due to ionizing radiation increases linearly with effective radiation dose at a rate of 5.5% per sievert. If this linear model is correct, then natural background radiation is the most hazardous source of radiation to general public health, followed by medical imaging as a close second. Other stochastic effects of ionizing radiation are teratogenesis, cognitive decline, and heart disease. The table below shows radiation
Biological effects of radiation on the epigenome epigenetic up-regulation of genes. A similar mechanism involves the ataxia telangiectasia mutated (ATM) serine/threonine kinase which is an enzyme involved in the repair of double stranded breaks caused by ionizing radiation. ATM phosphorylates KAP1 which causes the heterochromatin to relax, allowing increased transcription to occur. The DNA mismatch repair gene (MSH2) promoter has shown a hypermethylation pattern when exposed to ionizing radiation. Reactive oxygen species induce the oxidization of deoxyguanosine into 8-hydroxydeoxyguanosine (8-OHdG) causing a change in chromatin structure. Gene promoters that contain 8-OHdG deactivate the chromatin by inducing trimethyl-H3K27 in the genome. Other enzymes such as transglutaminases (TGs) control