<unk>  is a stochastic effect of radiation, meaning it is an unpredictable event. The probability of occurrence increases with effective radiation dose, but the severity of the<unk>  is independent of dose. The speed at which<unk>  advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the person is exposed. This contrasts with the deterministic effects of acute radiation syndrome which increase in severity with dose above a threshold.<unk>  starts with a single cell whose operation is disrupted. Normal cell operation is controlled by the chemical structure of DNA molecules, also called chromosomes. When radiation deposits enough energy in organic tissue to cause ionization, this tends to break molecular bonds, and thus alter the molecular structure of the irradiated molecules. Less energetic radiation, such as visible light, only causes excitation, not ionization, which is usually dissipated as heat with relatively little chemical damage. Ultraviolet light is usually categorized as non-ionizing, but it is actually in an intermediate range that produces some ionization and chemical damage. Hence the carcinogenic mechanism of ultraviolet radiation is similar to that of ionizing radiation. Unlike chemical or physical triggers for<unk> , penetrating radiation hits molecules within cells randomly. Molecules broken by radiation can become highly reactive free radicals that cause further chemical damage. Some of this direct and indirect damage will eventually impact chromosomes and epigenetic factors that control the expression of genes. Cellular mechanisms will repair some of this damage, but some repairs will be incorrect and some chromosome abnormalities will turn out to be irreversible. DNA double-strand breaks (DSBs) are generally accepted to be the most biologically significant lesion by which ionizing radiation causes<unk> . In vitro experiments show that ionizing radiation cause DSBs at a rate of 35 DSBs per cell per Gray, and removes a portion of the epigenetic markers of the DNA, which regulate the gene expression. Most of the<unk>  DSBs are repaired within 24h after exposure, however, 25% of the repaired strands are repaired incorrectly and about 20% of fibroblast cells that were exposed to 200mGy died within 4 days after exposure. A portion of the population possess a flawed DNA repair mechanism, and thus suffer a greater insult due to exposure to radiation. Major damage normally results in the cell dying or being unable to reproduce. This effect is responsible for acute radiation syndrome, but these heavily damaged cells cannot become<unk> ous. Lighter damage may leave a stable, partly functional cell that may be capable of proliferating and eventually developing into<unk> , especially if tumor suppressor genes are damaged. The latest research suggests that mutagenic events do not occur immediately after irradiation. Instead, surviving cells appear to have acquired a genomic instability which causes an increased rate of mutations in future generations. The cell will then progress through multiple stages of neoplastic transformation that may culminate into a tumor after years of incubation. The neoplastic transformation can be divided into three major independent stages: morphological changes to the cell, acquisition of cellular immortality (losing normal, life-limiting cell regulatory processes), and adaptations that favor formation of a tumor. In some cases, a small radiation dose reduces the impact of a subsequent, larger radiation dose. This has been termed an 'adaptive response' and is related to hypothetical mechanisms of hormesis. A latent period of decades may elapse between radiation exposure and the detection of<unk> . Those<unk> s that may develop as a result of radiation exposure are indistinguishable from those that occur naturally or as a result of exposure to other carcinogens. Furthermore, National<unk>  Institute literature indicates that chemical and physical hazards and lifestyle factors, such as smoking, alcohol consumption, and diet, significantly contribute to many of these same diseases. Evidence from uranium miners suggests that smoking may have a multiplicative, rather than additive, interaction with radiation. Evaluations of radiation's contribution to<unk>  incidence can only be done through large epidemiological studies with thorough data about all other confounding risk factors.
Radiation-induced cancer
Chronic radiation syndrome
Radiation burn
Spaceflight radiation carcinogenesis
Radiation damage
Metastatic breast cancer
Senile osteoporosis
Bone metastasis