Chronic Leukemias and Multiple Myeloma

Amy M. Pick

LEARNING OBJECTIVES

Upon completion of the chapter the reader will be able to:

1. Explain the role of the Philadelphia chromosome (Ph) in the pathophysiology of chronic myelogenous leukemia (CML)

2. Describe the natural history of CML.

3. Identify the clinical signs and symptoms associated with CML.

4. Discuss treatment options for CML with special emphasis on tyrosine kinase inhibitors.

5. Describe the clinical course of chronic lymphocytic leukemia (CLL).

6. Describe patients who may be observed without treatment and those who receive aggressive treatment for CLL.

7. Discuss the various treatment options available for CLL.

8. Describe the clinical presentation of multiple myeloma.

9. Discuss treatment options available for multiple myeloma.

key concepts

The Philadelphia chromosome (Ph) is a chromosomal translocation responsible for chronic myelogenous leukemia (CML).

The Ph results in the formation of an abnormal fusion gene, BCR-ABL, which encodes an overly active tyrosine kinase.

Allogeneic stem cell transplantation is the only curative treatment option for CML.

Imatinib is a tyrosine kinase inhibitor used as first-line therapy in patients with CML.

Dasatinib and nilotinib are second-generation tyrosine kinase inhibitors used to overcome imatinib resistance or intolerance.

® Chronic lymphocytic leukemia (CLL) can have a variable disease course but most patients survive for many years.

'©' Chemotherapy does not improve overall survival in early-stage CLL.

® Fludarabine-based chemotherapy is commonly used as first-line therapy for younger patients with CLL.

O Autologous transplant either as a single or double transplant offers younger patients with myeloma longer disease-free survival.

® Newer therapies for multiple myeloma including thalidomide, lenalidomide, and bortezomib in combination with dexamethasone produce major responses.

introduction

Several diseases comprise chronic leukemia. The two most common forms are chronic myelogenous leukemia (CML) and chronic lymphocytic leukemia (CLL). The slower progression of the disease contrasts it from acute leukemia, with the survival of chronic leukemia often lasting several years without treatment. This chapter will cover CML and CLL. There will also be a discussion of multiple myeloma and a brief discussion of Waldenstrom macroglobulinemia.

chronic myelogenous leukemia

CML is a hematological cancer that results from an abnormal proliferation of an early myeloid progenitor cell.1 The clinical course of CML has three phases: chronic phase, accelerated phase, and blast crisis. Chemotherapy can be used to control WBC counts in the chronic phase but as CML slowly progresses the cancer becomes resistant to treatment. Blast crisis resembles acute leukemia and immediate aggressive treatment is required. Table 96-1 describes each of the phases of CML.

Table 96-1 Clinical Course of CML

Median Duration

Phase_Characteristics_(With Treatment)

Chronic blegated WBC 4-6 years4

Responsive to treatment

Accelerated blegated WBC months

Unresponsive to treatment Inc* eased symptoms

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