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Curing childhood acute myeloid leukemia (AML) at the half‐way point: Promises to keep and miles to go before we sleep
Author(s) -
Woods William G.
Publication year - 2005
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.20646
Subject(s) - medicine , myeloid leukemia , disease , leukemia , oncology , population , clinical trial , childhood leukemia , intensive care medicine , pediatrics , lymphoblastic leukemia , environmental health
Childhood and adolescent acute myeloid leukemia (AML) is traditionally one of the hardest childhood cancers to successfully treat and had an overall survival well under 10% in the 1960s. Initial progress was made by three major events: (1) active chemotherapeutic agents were identified which led to remissions for the first time in this disease; (2) cooperative groups were instituted leading to important clinical trials; and (3) several single institutions began experimenting with the role of allogeneic matched sibling donor (MSD) BMT as effective intensification. Over the last 25 years, the cure rate has improved from <20% to 50% or higher. Most of the clinical research during this time of great advancement focused on two major themes: (1) the role of aggressive induction therapy in not only improving CR rates but in post‐remission outcomes; and (2) the role of aggressive post‐remission therapy in further improving survival, with an emphasis on high‐dose Ara C‐based chemotherapy, BMT, and supportive care. But we have “miles to go before we sleep.” Some of the challenges that will lead to ongoing reduction of population‐based mortality for AML through young adulthood include: (1) improving access of adolescents to pediatric AML therapy; (2) stratification by prognostic factors; (3) individualized therapy based on individual genetics and leukemia cell biology; (4) and the use of novel therapies including targeted immuno‐conjugates and “small molecules” which disrupt abnormal signal transduction pathways. This brief review looks at both the advances over the last three decades as well as discusses the challenges moving forward for ultimately curing all children with this disease. © 2005 Wiley‐Liss, Inc.