Progression of CML to acute leukemia (blast crisis) in humans has been associated with acquisition of secondary chromosomal translocations, including the t(7;11)(p15;p15) resulting in the NUP98/HOXA9 fusion protein.     ///    We demonstrate that BCR/ABL cooperates with NUP98/HOXA9 to cause blast crisis in a murine model.     ///    "These experiments document cooperative effects between constitutively activated tyrosine kinases, which confer proliferative and survival properties to hematopoietic cells, with mutations that impair differentiation, such as the NUP98/HOXA9, giving rise to the acute myeloid leukemia (AML) phenotype. "    ///    "The phenotype depends both on expression of BCR/ABL and NUP98/HOXA9, but tumors retain sensitivity to the ABL inhibitor STI571 in vitro and in vivo. "    ///    A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9.. 