ABSTRACT
Hematological malignancies originate in the bone marrow, lymph nodes, and/or other lymphoid tissue with immune function. Interpretation of much of the literature on occupation and risk of chronic lymphoblastic leukemia is complicated by lack of homogeneity of the lymphopoietic disorders studied and lack of validation of diagnosis in most studies. The most important epidemiological investigation quantifying cancer risks associated with radiation exposures is the long-term follow-up of the Japanese atomic bomb survivors. Because the etiology of most hematological malignancies is believed to be multifactorial, common genetical variants, including single-nucleotide polymorphisms, may influence susceptibility. Postulated genetical mechanisms for familial leukemia include inherited germline mutations, primary immunolo-gical alterations, sharing of common haplotypes, and/or consanguinity. Understanding of etiology requires recognition of the characteristic genetic instability and highly variable history of the normal life cycle of lymphocytes, which undergo genetic recombination and mutation to generate high-affinity antibodies.
