Genetic, endocrine, and viral aspects of AKR leukemogenesis.
In the AKR strain of mice a high incidence of spontaneous lymphoid leukemia develops before 12 months of age. Genetic, viral, and endocrine factors interact during development to produce the syndrome. Many of the deficiencies of AKR mice are associated with gene action in chromosome 17, at or near the major histocompatibility locus. It is suggested that low steroid levels and high thyroxin levels during an early period of development are an essential part of the syndrome. Specifically, induction of a polymerase enzyme and regulation of the extent of its action by hormones are postulated to favor appearance of C-type particles and accumulation of a population of undifferentiated lymphoid stem cells. Immunodeficiency and leukemic transformation result.
D000818:Animals; D000917:Antibody Formation; D002874:Chromosome Mapping; D012321:DNA-Directed RNA Polymerases; D004967:Estrogens / Q000502:physiology; D012739:Gonadal Steroid Hormones / Q000502:physiology; D009052:Leukemia Virus, Murine / Q000502:physiology; D007945:Leukemia, Lymphoid / Q000209:etiology / Q000382:microbiology / Q000503:physiopathology / Q000662:veterinary*; D008214:Lymphocytes / Q000502:physiology; D051379:Mice; D008806:Mice, Inbred AKR; D012376:Rodent Diseases / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology; D013950:Thymus Gland / Q000503:physiopathology
D004967:Estrogens; D012739:Gonadal Steroid Hormones; D012321:DNA-Directed RNA Polymerases