Abstract

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder that progresses in a multistep fashion. The number of genetic lesions necessary to generate disease progression is unknown, but the clinical heterogeneity of patients and the wide variety of observed secondary changes suggest that construction of a unified theory of progression is impossible and that probably multiple genomic alterations are required to induce the phenotype of blast crisis. The transition between chronic phase and blast crisis is associated with marked functional changes, making CML a unique model for studying the process of leukemogenesis in humans.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call