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Blood, 15 May 2002, Vol. 99, No. 10, pp. 3801-3805
NEOPLASIA
In utero origin of t(8;21) AML1-ETO translocations in
childhood acute myeloid leukemia
Joseph L. Wiemels,
Zhijian Xiao,
Patricia A. Buffler,
Ana T. Maia,
Xiaomei Ma,
Brian M. Dicks,
Martyn T. Smith,
Luoping Zhang,
James Feusner,
John Wiencke,
Kathy Pritchard-Jones,
Helena Kempski, and
Mel Greaves
From the Laboratory for Molecular Epidemiology,
Department of Epidemiology and Biostatistics, University of California
San Francisco; Leukaemia Research Fund Centre, Institute of Cancer
Research, and the Leukaemia Research Fund Centre for Childhood
Leukaemia, Molecular Haematology and Cancer Biology Unit, Institute of
Child Health, London, United Kingdom; School of Public Health,
University of California Berkeley; Department of Hematology/Oncology,
Children's Hospital Oakland, CA; Children's Cancer Unit, Royal
Marsden Hospital, Sutton, Surrey, United Kingdom.
Recent reports have established the prenatal origin of
leukemia translocations and resultant fusion genes in some patients, including MLL-AF4 translocations in infants and
TEL-AML1 translocations in children. We now report evidence
for the prenatal origin of a translocation in childhood acute myeloid
leukemia (AML). The t(8;21) AML1-ETO translocations
were sequenced at the genomic level in 10 diagnostic leukemia samples
from children with available neonatal Guthrie blood spots. Clonotypic
genomic AML1-ETO sequences were detected in the Guthrie
spots for 5 individuals, providing unambiguous evidence of prenatal
origin in these cases. Two of these patients were older than 10 years
of age at diagnosis, indicative of a protracted postnatal latency.
Three of the patients were assessed for the persistence of genomic
fusion sequences in complete clinical remission samples and were found
to be positive. These data indicate that t(8;21) in childhood AML can
arise in utero, possibly as an initiating event in childhood AML, and
may establish a long-lived or stable parental clone that requires
additional secondary genetic alterations to cause leukemia.
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