KRAS2 oncogene overexpression in myelodysplastic syndrome with translocation 5;12

Arun Srivastava, H. Scott Boswell, Nyla A. Heerema, Piruz Nahreini, Richard C. Lauer, Asok C. Antony, Ronald Hoffman, Guido J. Tricot

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


The factors that initiate and maintain the abnormal hematopoietic clone in the myelodysplastic syndromes (MDS) remain largely unknown. We describe a patient with MDS associated with an abnormal karyotype, 46,XY,t(5;12)(q31;p12). According to the FAB cooperative group classification, the patient was classified as chronic myelomonocytic leukemia. Because of the particular chromosomal translocation, the structure-function relationship of three genes relevant to the translocation breakpoints, CSF2, FMS, and KRAS2, was studied in bone marrow and peripheral blood lymphocytes in this patient. No major structural alterations were observed at these three genetic loci. Although the levels of expression of the CSF2 and FMS genes remained unaltered, the KRAS2 oncogene was overexpressed approximately six-fold in bone marrow cells from the MDS patient compared with normal donors. We postulate that the RAS oncogene activation may be instrumental in the genesis of MDS.

Original languageEnglish (US)
Pages (from-to)61-71
Number of pages11
JournalCancer Genetics and Cytogenetics
Issue number1
StatePublished - Oct 1 1988

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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