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What Is the Optimal Therapy for Childhood AML?

What Is the Optimal Therapy for Childhood AML?

Improvement in pediatric acute myelogenous leukemia (AML) over the past 30
years has been only modest. Although rates of complete remission induction have
climbed steadily to 85% or 90%, cure rates remain in the 50% to 60% range. These
figures may inspire envy from medical oncologists treating adults with AML, but
they lag far behind the successes in treating pediatric acute lymphocytic
leukemia (ALL).

In their review of the modern therapy experience in pediatric AML, Drs. Loeb
and Arceci have done an admirable job in providing a comprehensive synthesis of
the therapeutic experience to date. They summarize the extensive experience of
the most important single and multicenter trials, including those of the
American, British, Scandinavian, and other European groups, and arrive at
several general conclusions.

Key Findings

First, the known active agents—cytarabine, the anthracyclines, etoposide,
and the alkylating agents—appear to generate optimal results when applied in
both dose- and schedule-intensive strategies during the first several months of
therapy. Second, short, intensive therapies (ie, 1 to 2 years) are adequate to
cure many patients, whereas prolonged therapies (intensive or not) appear only
to add to toxicity without a corresponding improvement in efficacy.

Third, with the notable exception of the Medical Research Council’s MRC AML10
trial, allogeneic bone marrow transplantation has been shown to be more
effective than chemotherapy alone, but outcomes after autologous transplantation
have generally been found to be the same or worse than those with chemotherapy
alone. The emerging role of biological and cytogenetic features in defining
different prognostic groups is also highlighted.

New Approaches

In their discussion of new therapies, the authors outline the promise
attendant to several newer approaches being studied. These include
differentiation induction with retinoids and arsenic trioxide (Trisenox), in
both acute promyelocytic (APL) and other FAB subgroups; inhibition of DNA
methylation and acetylation and of tyrosine kinase; and several immune-based
strategies using exogenous antibodies, tumor vaccines, or cytokine-treated AML
blasts as antigen-presenting dendritic cells.

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