Elizabeth S. Rich, Cara A. Rosenbaum, and Wendy Stock
In acute lymphoblastic leukemia (ALL), normal hematopoiesis is suppressed by accumulation in the bone marrow of clonal, malignant lymphoblasts. Arrested at various stages of development, different subtypes of ALL are characterized by distinct immunophenotypic, cytogenetic, and molecular features. In contrast to pediatric ALL, where cure rates approach 80%, only one-third of adult patients with ALL achieve long-term disease-free survival (DFS). To improve the outcome of patients with adult ALL, insight gained from the characterization of ALL has led to a risk-adapted approach to therapy.1 Further understanding of the biology of this disease will refine this risk-adapted approach, with the ultimate goal of improving the cure rates of adult patients with ALL.
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