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Hematologic malignancies were the first human cancers to be studied in depth at the molecular level, and recent years have seen important advances in treatment. This comprehensive reference book covers the full range of hematologic malignancies, including all subtypes of leukemias, lymphomas, and plasma cell dyscrasias. Authored by internationally known experts, each chapter emphasizes diagnostic work-up, staging, and therapeutic approaches. Up-to-date hematopathology, treatment, and outcomes data are presented in a way which is directly applicable to patient care. Highly illustrated with color images, graphs, flowcharts and treatment algorithms, the book is perfect for quick clinical reference as well as providing detailed reference lists for further study. With its authoritative and practical focus and visually stimulating presentation, this is a key text for hematology and oncology fellows, physicians, oncology nurses, physician assistants and other healthcare workers in the field of oncology.
Elias Jabbour, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA,
Hagop M. Kantarjian, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA,
Jorge E. Cortés, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Chronic myeloid leukemia (CML) is a relatively rare disease but is one of the most extensively studied and best understood neoplasms, and one for which a direct gene link has been found. CML is characterized by a balanced genetic translocation, t(9;22)(q34;q11.2), involving a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This rearrangement is known as the Philadelphia chromosome (Ph). The molecular consequence of this translocation is the generation of a BCR-ABL fusion oncogene, which in turn translates into a Bcr-Abl oncoprotein. Bcr-Abl displays transforming activity owing to its constitutive kinase activity, which results in multiple signal transduction pathways leading to uncontrolled cell proliferation and reduced apoptosis and resulting in the malignant expansion of pluripotent stem cells in bone marrow. CML is usually diagnosed in the chronic phase (CP) and, if not treated, progresses through an accelerated phase (AP) to a terminal blastic phase (BP).
Incidence, epidemiology, and etiology
CML accounts for 15% to 20% of cases of leukemia in the United States. There is a slight male preponderance. Its annual incidence is about 1 to 2 cases per 100,000 individuals. About 5000 to 6000 cases of CML are diagnosed annually. This incidence has not changed over the past few decades, and increases with age. The median age at CML diagnosis is 55 to 60 years; it is uncommon in children and adolescents. Before imatinib therapy, the prevalence of CML was about 25,000 cases in the United States.
Stefan H. Faderl, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA,
Guillermo Garcia-Manero, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA,
Hagop M. Kantarjian, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Myelodysplastic syndromes (MDS) are a heterogeneous group of hematopoietic stem cell disorders which are distinguished by cytopenias in the face of hypercellular marrows and dysplastic hematopoietic cell lines. Up into the 1970s MDS have been called “preleukemia” expressing the proximity of MDS to acute myeloid leukemia (AML), and their capacity to evolve into AML over time. Although MDS is the currently accepted term, the pathophysiology of MDS varies widely extending from abnormalities of apoptosis and differentiation to proliferation and maturation arrest. It is nowadays also better understood that there are notable differences between MDS and AML, a separation which is also underlined by the clinical manifestations and prognosis of MDS, which are primarily determined by cytopenias and not leukemic transformation. The complexity of pathophysiology and resultant heterogeneity of prognosis have led to several recent attempts to fine tune criteria for diagnosis and classification. In addition, recent years have also seen important advances of treatment with respect to hematopoietic growth factors, iron chelation, and particularly epigenetic therapy and immunomodulatory inhibitory derivatives (e.g., lenalidomide). These developments have made the care of patients with MDS more demanding but at the same time more satisfying as the possibilities for patients with MDS are now larger than before.