Chronic myeloid leukemia

This chapter summarizes the knowledge regarding the molecular biology of chronic myeloid leukemia (CML) and the treatment modalities, including novel breakpoint cluster region-v-abl Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1) tyrosine kinase inhibitors (TKIs). The discovery that BCR-ABL1 plays a pivotal role in the pathogenesis of CML set the stage for the development of therapeutic strategies aimed at inhibiting this kinase and its downstream signals. In CML-blastic phase the use of TKI in combination with chemotherapy is superior to single-agent TKI or chemotherapy alone, even after failure of TKI or chemotherapy. The transition from CML-chronic phase to CML-accelerated phase is subclinical and laboratory monitoring is necessary to detect disease progression. The different CML phases predict for very different survival probabilities. However, the prognosis is variable among patients in the same phase of the disease. Several patient and disease characteristics have been found to be prognostically useful and have been used to generate prognostic models.