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Absence of oncogene amplifications and occasional activation of N-ras in
lymphoblastic leukemia of childhood
S Rodenhuis, JL Bos, RM Slater, H Behrendt, M van 't Veer and LA Smets
To examine whether determination of (1) the copynumber or restriction
pattern of certain oncogenes or (2) the mutational activation of the N- ras
gene might contribute to the risk classification of acute lymphoblastic
leukemia of childhood (ALL), we investigated DNA isolated from lymphoblasts
of untreated patients. Restriction enzyme analysis of cellular oncogenes
was performed on DNA of 25 patients. No rearrangements could be
demonstrated within or near the genes c-myc, c- myb, c-abl, bcr, c-Ki-ras,
and N-ras. No amplifications of these genes nor of N-myc or c-Ha-ras were
present. Eight of 21 patients were heterozygote for "rare" Ha-ras allelic
restriction fragments that have been associated with an increased risk of
developing a malignancy. These patients were clinically indistinguishable
from patients lacking these fragments. The breakpoint cluster region (bcr)
that is rearranged in all patients with Philadelphia chromosome positive
chronic myeloid leukemia, was normal in all cases, including at least one
patient with Philadelphia chromosome positive ALL. A 2.8 kb HindIII
fragment of a hitherto unknown gene or pseudogene related to v-myb probably
derives from the Y chromosome. Nineteen patients were examined for point
mutations in the N-ras gene, using a novel synthetic oligonucleotide
hybridization assay. In two patients activating point mutations were
present, both in positions 1 of the 12th codon. Both patients were somewhat
older than the others (16 and 11 years), had L2 morphology, and were shown
to have high growth fractions of tumor in their bone marrow.
Volume 67,
Issue 6,
pp. 1698-1704,
06/01/1986
Copyright © 1986 by The American Society of Hematology
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