Ras activation in myelodysplastic syndromes: Clinical and molecular study of the chronic phase of the disease

C. Melani, A. Haliassos, J. C. Chomel, M. Miglino, A. M. Ferraris, G. F. Gaetani, J. C. Kaplan, A. Kitzis

Research output: Contribution to journalArticlepeer-review

Abstract

We studied N-ras and Ki-ras point mutations respectively at codons 12-13 and 12 in 15 patients with myelodysplastic syndromes (MDS) using the polymerase chain reaction (PCR) method for DNA amplification, and slot blot hybridization to allele specific oligonucleotide (ASO) probes. We analysed peripheral blood and bone marrow samples collected at diagnosis and repeatedly during the chronic phase of the disease to define when the activation occurred and in which haemopoietic cell populations, in order to establish possible relationships between clinical and molecular features. In three cases the N-ras oncogene was mutated at codon 12 in every cell population, both at diagnosis and throughout the chronic phase. Point mutations were not seen at the 12 codon of the Ki-ras oncogene. In patients lacking activated ras oncogene at diagnosis, mutations were not discovered during the entire period of observation. Therefore in our cases disease progression and leukaemia transformation did not correlate with the presence of the activated N-ras. Our data suggest that ras activation occurs early in the pathogenesis of MDS and involves a haemopoietic progenitor with multiple differentiative capacity, without however conferring an apparent proliferative advantage on its progeny.

Original languageEnglish
Pages (from-to)408-413
Number of pages6
JournalBritish Journal of Haematology
Volume74
Issue number4
Publication statusPublished - 1990

ASJC Scopus subject areas

  • Hematology

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