Figure 4.
Figure 4. AMN107 prolongs survival of animals with myeloproliferative disease induced by TEL-PDGFRβ or FIP1L1-PDGFRα in a murine bone marrow transplantation model. Bone marrow cells of donor mice were transduced with retrovirus expressing either TEL-PDGFRβ (A) or FIP1L1-PDGFRα (B) and transplanted into lethally irradiated recipients. Animals were monitored for appearance of disease and were killed when moribund. The plot shows cumulative disease-free survival of mice that received a transplant with cells expressing each fusion kinase and treated with either AMN107 (75 mg/kg/d) or placebo, starting at day 11 after transplantation. An increase in survival in the AMN107-treated group was statistically significant for both TEL-PDGFRβ and FIP1L1-PDGFRα (P < .001); n = 8 for TEL-PDGFRβ and n = 5 for FIP1L1-PDGFRα.

AMN107 prolongs survival of animals with myeloproliferative disease induced by TEL-PDGFRβ or FIP1L1-PDGFRα in a murine bone marrow transplantation model. Bone marrow cells of donor mice were transduced with retrovirus expressing either TEL-PDGFRβ (A) or FIP1L1-PDGFRα (B) and transplanted into lethally irradiated recipients. Animals were monitored for appearance of disease and were killed when moribund. The plot shows cumulative disease-free survival of mice that received a transplant with cells expressing each fusion kinase and treated with either AMN107 (75 mg/kg/d) or placebo, starting at day 11 after transplantation. An increase in survival in the AMN107-treated group was statistically significant for both TEL-PDGFRβ and FIP1L1-PDGFRα (P < .001); n = 8 for TEL-PDGFRβ and n = 5 for FIP1L1-PDGFRα.

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