The Oncologist, Vol. 4, No. 3, 225-240,
June 1999
© 1999 AlphaMed Press
Leukemia in Infants
Carolyn A. Felix,
Beverly J. Lange
Division of Oncology, The Children's Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Correspondence:
Carolyn A. Felix, M.D., Division of Oncology, Abramson Research Center, Room 902B, The Children's Hospital of Philadelphia, 324 South 34th Street, Philadelphia, Pennsylvania 19104-4318, USA. Telephone: 215-590-2831; Fax: 215-590-3770; e-mail: felix{at}email.chop.edu
Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) in infants have in common a high incidence of translocations of the MLL gene at chromosome band 11q23. Similar translocations occur in leukemias associated with chemotherapies that target DNA topoisomerase II. MLL has numerous different partner genes. The role of the many MLL fusion proteins in leukemogenesis is not yet understood. The t(4;11) translocation, the most common translocation in infant ALL, adversely affects the outcome. Additional genetic changes, especially Ikaros alterations, are found in infant ALL. Other forms of myeloid leukemia in infants present as myelodysplastic and myeloproliferative syndromes, which may be associated with constitutional disorders. This review will consider all leukemia in infants, but will focus on leukemias with MLL gene translocations.
Key Words. Acute myeloid leukemia (AML) • Acute lymphoblastic leukemia (ALL) • MLL gene • Down syndrome • Constitutional disorder • Clinical • Molecular biology • Epidemiology • DNA topoisomerase II
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Copyright © 1999 by AlphaMed Press.
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