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

BMC Cancer. 2006 Apr 21:6:100. doi: 10.1186/1471-2407-6-100.

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / blood*
  • Bone Marrow Cells / chemistry
  • Child
  • Child, Preschool
  • Clone Cells / chemistry
  • Cohort Studies
  • Core Binding Factor Alpha 2 Subunit / blood
  • Core Binding Factor Alpha 2 Subunit / genetics
  • DNA, Neoplasm / blood*
  • Female
  • Fetal Blood / chemistry*
  • Gene Duplication
  • Gene Rearrangement, B-Lymphocyte*
  • Gene Rearrangement, T-Lymphocyte*
  • Humans
  • Infant
  • Infant, Newborn
  • Leukemia, Myeloid / blood
  • Leukemia, Myeloid / embryology*
  • Leukemia, Myeloid / epidemiology
  • Leukemia, Myeloid / genetics
  • Male
  • Myeloid-Lymphoid Leukemia Protein / blood
  • Myeloid-Lymphoid Leukemia Protein / genetics
  • Neonatal Screening
  • Neoplasm Proteins / blood
  • Neoplasm Proteins / genetics
  • Oncogene Proteins, Fusion / blood*
  • Oncogene Proteins, Fusion / genetics
  • Polymerase Chain Reaction
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / embryology*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • RUNX1 Translocation Partner 1 Protein
  • Tandem Repeat Sequences
  • fms-Like Tyrosine Kinase 3 / blood
  • fms-Like Tyrosine Kinase 3 / genetics

Substances

  • AML1-ETO fusion protein, human
  • Biomarkers, Tumor
  • CBFbeta-MYH11 fusion protein
  • Core Binding Factor Alpha 2 Subunit
  • DNA, Neoplasm
  • MLL-AF10 fusion protein, human
  • MLL-AF6 fusion protein, human
  • Neoplasm Proteins
  • Oncogene Proteins, Fusion
  • RUNX1 Translocation Partner 1 Protein
  • TEL-AML1 fusion protein
  • promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  • Myeloid-Lymphoid Leukemia Protein
  • FLT3 protein, human
  • fms-Like Tyrosine Kinase 3