Diagnosis and treatment of childhood acute lymphoblastic leukemia

Abstract

Leukemia is the most common pediatric cancer. Acute lymphoblastic leukemia (ALL) is the most prevalent subtype, accounting for 75-80 % of all cases. Leukemias arise from genetic changes that occur in a single progenitor cell at various stages of maturation, resulting in a clonal expansion. The single-cell origin of ALL is demonstrated clearly by the finding of clonal rearrangements of T-cell receptor (TCR) or immunoglobulin genes [1]. ALL cells reflect, at least in part, the immunophenotypic and genetic characteristics of committed B- or T-lymphoid precursors; although they do not proliferate as rapidly as their normal counterparts [2], inability to differentiate and resistance to cell death lead to their buildup. By the time of diagnosis, ALL cells have usually occupied much of the bone marrow microenvironment at the expenses of normal hematopoietic cells, resulting in anemia, thrombocytopenia, and/or neutropenia.