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Blood, Vol. 96 No. 3 (August 1), 2000:
pp. 1094-1099
TEL/AML1 gene fusion is related to in vitro drug sensitivity for
L-asparaginase in childhood acute lymphoblastic
leukemia
Nicole L. Ramakers-van Woerden,
Rob Pieters,
Annemarie H. Loonen,
Isabelle Hubeek,
Ellen van Drunen,
H. Berna Beverloo,
Rosalyn M. Slater,
Jochen Harbott,
Jeanette Seyfarth,
Elisabeth R. van Wering,
Karel Hählen,
Kjeld Schmiegelow,
Gritta E. Janka-Schaub, and
Anjo J. P. Veerman
From the Department of Pediatric Hematology/Oncology, University
Hospital Vrije Universiteit, Amsterdam; the Division of
Oncology/Hematology, Sophia Children's Hospital, Erasmus University,
Rotterdam; the Department of Cell Biology and Genetics and the
Department of Clinical Genetics, Erasmus University, Rotterdam; the
Dutch Childhood Leukemia Study Group, The Hague, The Netherlands;
Oncogenetic Laboratory, Children's Hospital, University of Giessen;
the COALL Study Group, Hamburg, Germany; Tissue Typing Laboratory and
the Department of Pediatric Hematology/Oncology, Rigshospitalet,
Copenhagen, Denmark.
The t(12;21) translocation resulting in TEL/AML1 gene fusion is
present in approximately 25% of patients with precursor B-lineage pediatric acute lymphoblastic leukemia (ALL). Studies suggest an
association with a good prognosis; however, relapse can occur. We
studied the relation between t(12;21), determined by fluorescence in
situ hybridization or polymerase chain reaction, and in vitro drug
resistance, measured by the MTT assay, in childhood B-lineage ALL at
diagnosis. A total of 180 ALL samples were tested, 51 (28%) of which
were positive for t(12;21). The median LC50 values did not
differ significantly between TEL/AML1-positive and -negative samples
for prednisolone, dexamethasone, daunorubicin, thiopurines, epipodophyllotoxins, and 4-HOO-ifosfamide. However, the
TEL/AML1-positive patients were relatively more sensitive to
L-asparaginase (ASP; 5.9-fold; P = .029) and
slightly but significantly more resistant to vincristine (1.5-fold;
P = .011) and cytarabine (1.5-fold; P = .014).
After matching for unevenly distributed patient characteristics that is, excluding patients younger than 12 months, patients with
CD10-negative immature B-lineage ALL, patients with Philadelphia
chromosome, and patients who were hyperdiploid (more than 50 chromosomes) from the TEL/AML1 negative groupthe only remaining
difference was a relative sensitivity for ASP in the TEL/AML1-positive
samples (10.8-fold; P = .012). In conclusion, the presence of
TEL/AML1 gene fusion in childhood precursor B-lineage ALL does not seem to be associated with a high in vitro drug sensitivity, except for ASP,
indicating that these patients could benefit from treatment schedules with significant use of this drug.
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