Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence (Leukemia: lymphatic)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000648 | AKR/J | Level 2 |
| Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol. | ||
| 006099 | B6;129-Sfpi1tm1.2Dgt/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. Endogenous protein expression is unaffected by the loxP sequences flanking an upstream regulatory region (URE). When bred to mice with a cre recombinase gene under the control of a promoter of interest, the URE of the targeted gene is deleted in the tissue of interest. Deletion of this "floxed" URE may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and development of multiple cell lineages. | ||
| 006083 | STOCK Sfpi1tm1.3Dgt/J | Repository-Cryopreserved |
| Mice homozygous for this targeted deletion are viable and fertile as young animals. Mice on this stock (predominantly 129Sv) background often die between 3-8 months of age of a rapidly developing T cell lymphoma (64% penetrance) or between 6-12 months of acute myeloid lymphoma (AML) (29% penetrance). Homozygotes (termed PU.1 knockdown or UREdelta) have an 80% reduction of endogneous gene expression. This is associated with an accumulation of hematopoietic stem cell precursor cells and neutrophils in bone marrow and spleen. Bone marrow cells from homozygous mice have abnormal responses to myeloid cytokines, and malignant transformation is associated with clonal chromosomal abnormalities. Homozygous mice have abnormal B- and T-cell populations and lineage commitment. These mice may be useful in studing T cell lymphoma, AML and other cancers, transcription factors, and development of multiple cell lineages. Of note, the latency and penetrance of disease is slightly different from those
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