ABSTRACT
This chapter discusses various experimental observations related to the possible role of amplification of the break point cluster region (bcr)-abl fusion gene in the pathogenesis of chronic myelogenous leukemia (CML) and, in particular, in the progression of CML from chronic phase to blast crisis. The human c-abl cellular oncogene was originally identified by virtue of its homology to v-abl, the transforming gene of the Abelson murine leukemia virus. This virus is a recombinant of the Moloney murine leukemia virus genome and the normal mouse cellular c-abl gene. The evolution of CML from chronic phase to blast crisis is commonly associated with karyotypic changes, the most frequent of which is the development of two or more Ph chromosomes. This acquisition of multiple Ph chromosomes is noted in approximately 50% of blast crisis CML samples.
