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Abstract
The discovery of the Philadelphia chromosome as a marker for chronic myelogenous leukemia (CML) in 1960 represented an important scientific breakthrough (1). It established for the first time that a specific chromosomal abnormality was associated with a specific malignancy. Unfortunately, this major event did not translate into direct clinical benefits for patients with this disease. Over the next 20-25 years, our understanding continued to grow while our clinical approach remained essentially unchanged. We know that the Philadelphia chromosome is the result of a translocation (2) and we understand the nature of aberrant and complex translocations (3). A consistent molecular event associated with the Philadelphia chromosome has been characterized (4,5). We understand that Philadelphia-negative CML may have the same molecular basis as Philadelphia-positive CML (6) and the relationship between this disease and Philadelphia-positive acute lymphoblastic leukemia (ALL) has also been clarified (7,8).