The Biology and Pathogenesis of Chronic Myeloid Leukaemia

Abstract

Chronic myeloid leukaemia (CML) is a myeloproliferative disorder of the pluripotent stem cell. Understanding the molecular biology of CML began with the discovery of the Philadelphia (Ph) chromosome. This genomic abnormality is the result of a t(9;22) translocation, leading to the fusion oncogene, BCR-ABL1. The resulting protein is capable of hijacking a vast repertoire of cellular functions that drive myeloid hyperplasia, characteristic of the initial, chronic phase of the disease. However, the mechanisms of resistance and disease progression are less well defined. In this chapter, we explore the various pathways involved in the pathogenesis of CML and also the biological events underpinning progression to the more advanced stages of the disease.