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Mutation of Ki-ras and N-ras oncogenes in myelodysplastic syndromes
J Lyons, JW Janssen, C Bartram, M Layton and GJ Mufti
Department of Paediatrics 11, University of Ulm, FRG.
Somatic mutation of the N-ras oncogene occurs frequently in de novo acute
myeloid leukemia (AML). By virtue of their relation to AML, myelodysplastic
syndromes (MDS) provide an in vivo model of human leukemogenesis. By using
a strategy for analysis of gene mutation based on in vitro amplification of
target sequences by the polymerase chain reaction (PCR) and selective
oligonucleotide hybridization we analyzed the mutational status of codons
12, 13, and 61 of Ha-ras, K-ras, and N- ras in peripheral blood (PB) and/or
bone marrow (BM) in 34 cases of primary MDS. Mutations at codon 12 of
Ki-ras or N-ras were detected in three cases (9%): one of six cases of
refractory anemia with excess blasts (RAEB) and two of nine cases of
chronic myelomonocytic leukemia (CMML). The nucleotide substitution
differed in each. In all cases the mutant allele was detectable in PB
cells. A sustained hematologic remission was achieved after low-dose
cytarabine therapy in the case of RAEB. Neither case of CMML exhibited
signs of disease progression during follow-up at 7 and 12 months. In
contrast, four of 31 patients without the ras mutation underwent
transformation to AML within 12 months of genetic analysis. We conclude
that ras mutations in MDS are heterogeneous and may develop at an early
stage during the evolution of MDS. Their detection in PB cells illustrates
the potential utility of ras mutation as a clonal marker in myeloid
malignancy.
Volume 71,
Issue 6,
pp. 1707-1712,
06/01/1988
Copyright © 1988 by The American Society of Hematology
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