Open Access Research article

Prenatal origin of childhood AML occurs less frequently than in childhood ALL

Tatiana Burjanivova12, Jozef Madzo12, Katerina Muzikova12, Claus Meyer3, Bjoern Schneider3, Felix Votava4, Rolf Marschalek3, Jan Stary2, Jan Trka12 and Jan Zuna12*

Author Affiliations

1 CLIP – Childhood Leukaemia Investigation Prague, Czech Republic

2 Department of Pediatric Hematology and Oncology, Charles University Prague, 2nd Medical School, Czech Republic

3 Institute of Pharmaceutical Biology/DCAL, University of Frankfurt, Frankfurt/Main, Germany

4 Department of Pediatrics, Charles University Prague, 3rd Medical School, Czech Republic

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BMC Cancer 2006, 6:100  doi:10.1186/1471-2407-6-100

Published: 21 April 2006



While there is enough convincing evidence in childhood acute lymphoblastic leukemia (ALL), the data on the pre-natal origin in childhood acute myeloid leukemia (AML) are less comprehensive. Our study aimed to screen Guthrie cards (neonatal blood spots) of non-infant childhood AML and ALL patients for the presence of their respective leukemic markers.


We analysed Guthrie cards of 12 ALL patients aged 2–6 years using immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements (n = 15) and/or intronic breakpoints of TEL/AML1 fusion gene (n = 3). In AML patients (n = 13, age 1–14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers. Assay sensitivity determined using serial dilutions of patient DNA into the DNA of a healthy donor allowed us to detect the pre-leukemic clone in Guthrie card providing 1–3 positive cells were present in the neonatal blood spot.


In 3 patients with ALL (25%) we reproducibly detected their leukemic markers (Ig/TCR n = 2; TEL/AML1 n = 1) in the Guthrie card. We did not find patient-specific molecular markers in any patient with AML.


In the largest cohort examined so far we used identical approach for the backtracking of non-infant childhood ALL and AML. Our data suggest that either the prenatal origin of AML is less frequent or the load of pre-leukemic cells is significantly lower at birth in AML compared to ALL cases.