Advertisement

ras Mutations in Preleukaemia, in Patients Following Cytotoxic Therapy and in Normal Subjects

  • G. Carter
  • D. Hughes
  • N. Warren
  • A. Jacobs
  • J. Whittaker
  • E. Thomson
  • R. A. Padua
Part of the NATO ASI Series book series (NSSA, volume 220)

Abstract

Point mutations in members of the RAS gene family, NRAS, KRAS and HRAS, are a common molecular lesion in patients with acute myeloid leukaemia (AML). Approximately 30% of such patients show mutations (Bos, 1987; Farr et al., 1988) mostly in NRAS, although KRAS abnormalities are also seen. Mutations in HRAS are a rare abnormality in haemopoietic malignancies (Browett et al., 1989). A similar pattern of mutations is also seen in patients with the preleukaemic Myelodysplastic syndromes (MDS), where mutations have been detected in up to 41% of patients (Padua et al., 1988; Yunis et al., 1989). In MDS RAS mutation appears to be associated with poor prognosis in terms of an increased likelihood of transformation to acute leukaemia, and whilst RAS mutation can be detected in all subtypes of MDS (Padua et al., 1988), the highest incidence is seen those patients a monocytic phenotype (Padua et al., 1988; Yunis et al., 1989).

Keywords

KRAS Mutation Acute Myeloid Leukaemia Cytotoxic Therapy Patient Acute Myeloid Leukaemia Acute Lymphocytic Leukaemia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Bos, J. L. 1989, RAS Oncogenes in Human Cancer, Cancer Research, 49:4682.PubMedGoogle Scholar
  2. Browett, P. J., Yaxley, J. C. & Norton, J. D. 1989, Activation of Harvey RAS Oncogene by Mutation at Codon 12 is Very Rare in Haemopoietic Malignancies, Leukaemia, 3:86.Google Scholar
  3. Carter, G., Hughes, D. C., Clark, R. E., Whittaker, J. A., Jacobs, A. J. & Padua, R. A. 1990 RAS Mutations Following Cytotoxic Therapy for Lymphoma, Oncogene, 5:411.PubMedGoogle Scholar
  4. Farr, C.J., Saiki, R. K., Erlich, H. A., McCormick, F. & Marshall, C. J., 1988, Analysis of RAS Gene Mutations in Acute Myeloid Leukaemia by Polymerase Chain Reaction and Oligonucleotide Probes, Proc. Natl. Acad. Sci. (USA), 85:1629.CrossRefGoogle Scholar
  5. Levine, E.G & Bloomfield, C.D. 1986, Secondary Myelodysplastic Syndromes and Leukaemias, Clin. Haematol., 15:1037.PubMedGoogle Scholar
  6. Nag, A., Jones, J. A. & Smith, R. G., 1989, Point Mutation in C- Ha-ras Oncogene in Normal and Abnormal Cells, Lancet, 1:274.PubMedCrossRefGoogle Scholar
  7. Padua, R. A., Carter, G., Hughes, D. C., Gow, J., Farr, C. J., Oscier, D., McCormick, F., Smith, S., & Jacobs, A. J., 1988 RAS Mutations in Myelodysplasia Detected by Amplification, Oligonucleotide Hybridisation and Transformation, Leukaemia, 8:503.Google Scholar
  8. Vogelstein, B., Fearon, E. R., Hamilton, S. R., Preisinger, A. C., Willard, H. F., Michelson, A. M., Riggs, A. D. & Orkin, S. H., 1987. Clonal Analysis Using Recombinant DNA Probes from the X-Chromosome, Cancer Research. 47:4806.PubMedGoogle Scholar
  9. Yunis, J.J., Boot, A. J. M., Mayer, M. G., & Bos, J. L. 1989, Mechanisms of ras Mutation in Myelodysplastic Syndrome, Oncogene, 4:609.PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • G. Carter
    • 1
  • D. Hughes
    • 1
  • N. Warren
    • 1
  • A. Jacobs
    • 1
  • J. Whittaker
    • 1
  • E. Thomson
    • 2
  • R. A. Padua
    • 1
  1. 1.LRF Preleukaemia Unit, Department of HaematologyUniversity of Wales College of MedicineCardiffUK
  2. 2.Department of Child HealthLlandough HospitalPenarth, South Glam.UK

Personalised recommendations