Detection of Bcr-abl Rna as a Method of Predicting Relapse in Cml

Chronic myeloid leukemia (CML) accounts for twenty percent of the incidence of leukemia in adults. The disease begins as a chronic low grade leukemia but frequently progresses to an accelerated transformation stage and then to blast crisis. The driving force behind CML is the Philadelphia chromosome (Ph), a reciprocal translocation t(9;22)(q34;q11) which forms the BCR-ABL fusion gene. Although the opposite translocation gene ABL-BCR is clinically silent, the BCR-ABL gene results in a constitutively active tyrosine kinase protein which is responsible for regulation of cell growth and leukemic transformation. The BCR-ABL translocation is found in virtually 100% of adult CML patients as well as in 20-30% of adult and 3% of pediatric acute lymphoblastic leukemia (ALL) patients.