Reconstitution of mice with bone marrow cells expressing the SCL gene is insufficient to cause leukemia.

Rearrangement or translocation of the SCL gene is the most common genetic abnormality observed in human T-cell acute lymphocytic leukemia and results in the aberrant expression of SCL. To examine the oncogenic potential of this gene, an SCL-retrovirus was used to infect mouse bone marrow cells, which were then used to reconstitute C57/BL6 mice. Expression of SCL did not perturb the composition nor number of day 12 or day 13 colony forming unit-spleen. In total, 141 mice reconstituted with SCL-infected bone marrow and 103 control-mice were monitored for up to 2 years with no difference in survival, hematocrit, white cell count, or differential white cell count. As expected, from day 200 onwards, mice died due to radiation-induced thymomas; SCL provirus was not detected in these tumors. Thus, despite SCL being strongly implicated in the development of human leukemia, its enforced expression in mice using a retrovirus and bone marrow reconstitution was insufficient to generate leukemia.