Author/Authors :
Harder، نويسنده , , L. and Gesk، نويسنده , , S. and Martin-Subero، نويسنده , , J.I. and Merz، نويسنده , , H. and Hochhaus، نويسنده , , A. and Maaك، نويسنده , , E. and Feller، نويسنده , , A. and Grote، نويسنده , , W. and Siebert، نويسنده , , R. and Fetscher، نويسنده , , S.، نويسنده ,
Abstract :
We describe a patient initially diagnosed with a chronic myeloproliferative disorder in the accelerated phase. Cytogenetic analysis showed the presence of two independent clones. One clone contained a typical Philadelphia (Ph) chromosome due to t(9;22)(q34;q11), as the sole abnormality which was proven molecularly to result in the b2a2-BCR/ABL fusion. The other clone displayed a complex karyotype with several structural and numerical aberrations including trisomy 11 and 22 but lacking a t(9;22) or any other structural abnormalities involving chromosomes 9 and 22. Fluorescence in situ hybridization demonstrated that the t(9;22) was present only in cells with two copies of chromosomes 11 and 22. In contrast, cells with trisomies 11 and 22 lacked evidence for a BCR/ABL fusion. Based on the genetic findings, simultaneous chronic and acute myelocytic leukemias were diagnosed rather than a blastic phase of a chronic myelocytic leukemia.
