Faculty Research 1990 - 1999


The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency.

Document Type


Publication Date



Blotting-Northern, Blotting-Southern, Chromosome-Mapping, Crosses-Genetic, DNA-Neoplasm: ge, Female, Immunologic-Deficiency-Syndromes: ge, im, Lymphoma: ge, im, pa, Male, Mice, Mice-Inbred-NOD: ge, Mice-SCID: ge, Mouse-Leukemia-Viruses: ge, Phenotype, RNA: ge, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, Thymus-Gland: ab, Thymus-Neoplasms: ge, im, pa, Virus-Integration

JAX Source

Proc Natl Acad Sci U S A 1992 Apr 15;89(8):3290-4


DK36175, DK27722, AI30389, +


Homozygosity for the severe combined immunodeficiency (scid) mutation results in a block in T- and B-lymphocyte development. An unusually high incidence of spontaneous thymic lymphoma development was observed after transfer of this mutation from the C.B-17 congenic strain background onto the diabetes-susceptible nonobese diabetic (NOD) background. Thymomagenesis in the NOD-scid/scid mouse was associated with expression of an NOD mouse-unique endogenous ecotropic murine leukemia provirus locus (Emv-30, mapped to proximal region of chromosome 11) not expressed in the standard substrain NOD/Lt thymus. All tumors exhibited insertions of ecotropic proviruses, whereas only a subset also exhibited proviral integrations of mink cell focus-forming retrovirus. Neither class of retrovirus was associated with consistent integration into genes previously associated with activation of oncogenesis. We propose that the unusual features of T-cell ontogeny characteristic of the NOD inbred strain synergize with the scid-imparted block in thymocyte development, leading to activation of the NOD-unique Emv-30 to initiate thymomagenesis.

Please contact the Joan Staats Library for information regarding this document.