Chronic myelogenous leukemia (CML) is a type of cancer of white blood cells, myeloid cells, that are mutated and proliferate uncontrollably through three stages (chronic, accelerated, and blast crisis) and lead eventually to death. Cytogenetics showed the myeloid cells of CML patients usually also have a consistent chromosome translocation (the mutant event) between the long arms of chromosomes 9 and 22, t(9:22)(q34;q11). It is also known as the Philadelphia chromosome (Ph+). This translocation involves breaks in two genes, c-abl and bcr, on chromosomes 9 and 22, respectively. The fusion of the translocation breaks result in a chimeric gene, called bcr-abl, that contains exons 1 and/or 2 from bcr (this varies from patient to patient) and 2-11 from abl and it produces a chimeric protein (BCR-ABL or p185bcr-abl) that is transcribed like bcr and contains abl enzyme sequences. This chimeric protein has a tyrosine-kinase from the abl gene sequences that is unique to the CML mutant cell. The consistent, unregulated expression of this gene and its kinase product causes activation of a variety of intracellular signaling pathways, promoting the uncontrolled proliferative and survival properties of CML cells (the cancer). Thus the BCR-ABL tyrosine kinase enzyme exists only in cancer cells (and not in healthy cells) and a drug that inhibits this activity could be used to target and prevent the uncontrolled growth of the cancerous CML cells.