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Mouse Models To Determine The Cause Of Aggressive Leukemia

harles J. Sherr, M.D., Ph.D., a Howard Hughes Medical Institute investigator and co-chair of the St. Jude Department of Genetics and Tumor Cell Biology said that Arf acts as a safeguard against the cancer-causing effects of Bcr-Abl. The St. Jude team found that Arf is not inactivated in CML patients who respond to imatinib. But in case of ALL Arf gene is lost frequently and imatinib treatment is far less effective. This inactivation of Arf in ALL cells expressing the Bcr-Abl enzyme gives these cells a strong proliferative nature which might contribute to imatinib resistance. So the researchers used a virus-like piece of DNA to carry the Bcr-Abl oncogene into bone marrow-derived lymphocytes obtained from mice that either retained Arf or were previously engineered to lack this gene. These pre-B lymphocytes represent one type of white blood cell that can become cancerous and cause ALL.

The researchers then transplanted these transformed cells carrying Bcr-Abl back into normal mice. Animals that received transformed pre-B cells that had both copies of the Arf gene intact were highly resistant to disease development. However, mice injected with cells that carried Bcr-Abl and lacked Arf rapidly developed an aggressive form of ALL that could not be cured with high doses of imatinib. Richard T. Williams, M.D., Ph.D., a fellow in Sherr’s laboratory and the paper’s lead author said that tumor cells when removed from these resistant mice and treated with imatinib in cell cultures they were still very sensitive to this drug. Hence he said that the failure of imatinib to cure the mice depended on some substance in the animal that stimulated tumor cell replication or survival.

They soon found that it might be the B lymphocyte stimulating protein IL-7. It is produced in the bone marrow enhancing the proliferation of cultured leukemic cells removed from the mice and made the cells resistant to imatinib’s growth inhibitory effects. It binds to receptors on the su
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