Current Treatment Concepts of CML
A. A. Leitner,
M. C. Muller.
The elucidation of the triggering molecular mechanism of chronic myeloid leukemia gave rise to the development of imatinib, a tyrosine kinase inhibitor and a prototype of target-oriented drugs. Imatinib led to impressing response and survival rates and now represents the standard therapy of CML. However, a significant proportion of patients do not tolerate or fail to respond to imatinib treatment. Alternative therapies can be offered to those patients. The particular challenge of CML patient management is to recognize an impending imatinib failure by adequate surveillance and to know about therapeutic options to prevent progression of the disease to accelerated phase or blast crisis since these are more difficult to control. Targeted therapy with second-generation tyrosine kinase inhibitors should be used in synopsis with mutational analysis and the patients history. In this review we present current knowledge of diagnosis, monitoring and therapy strategies of patients with CML.
Keywords: Chronic myeloid leukemia, imatinib, dasatinib, nilotinib, BCR-ABL, mutation, rare disease, diagnosis, lymphoblastic, fatigue, weight loss, abdominal discomfort, splenomegaly, myeloproliferative neoplasm (MPN), polycythemia vera, thrombocythemia, Leukemia Virus, hematopoietic cells, blood counts, complete hematologic remission (CHR), malignant cells, histologic, cytologic, White blood cell count, fluorescence, hybridization (FISH), metaphases, Plasma Leve, intestinal absorption, metabolism, glycoprotein, hydroxyurea, arsenic, splenectomy, splenic irradiation, busulfan, pregnancy, ribonucleotide, tyrosine kinase inhibitors (TKI), antimetabolite cytarabine, monotherapy, autophosphorylation, bioavailability, phosphate-binding, nucleotide polymorphisms, DOSE, potency, pharmacokinetics, first line therapy, lymphoid, blood-brain barrier, toxicity, Stem Cell Transplantation (SCT), autologous SCT, chemotherapy, diabetes, electrocardiograms
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