The outline of a quantitative model is presented which can be used to derive the pathway from radiation-induced molecular damage, the DNA double strand break, to cellular effects such as cell killing, chromosomal aberrations and mutations and on to radiation-induced cancer. Evidence is provided to support the links in the chain which relate the different cellular end-points to each other and to cancer. The influence of differing dose rates and types of radiation on dose effect relationships are discussed. The extension to radiation induced cancer is made using a two mutation multi-step model for carcinogenesis and evidence is provided to support the assumption that radiation induced cancer arises from a somatic mutation. The dose response for radiation induced cancer is presented and various implications for radiation risks are outlined. The model is also extended to a consideration of deterministic effects by assuming that these effects arise as a result of multi-cell killing at high acute doses. The implications of the model for medical diagnostic radiology are discussed.