TY - JOUR
T1 - KRAS2 oncogene overexpression in myelodysplastic syndrome with translocation 5;12
AU - Srivastava, Arun
AU - Boswell, H. Scott
AU - Heerema, Nyla A.
AU - Nahreini, Piruz
AU - Lauer, Richard C.
AU - Antony, Asok C.
AU - Hoffman, Ronald
AU - Tricot, Guido J.
N1 - Funding Information:
Supported by American Cancer Society Institutional grant IN-161A (to A. S.), a Veterans Administration Merit Review Award (to H. S. B.), and grants 1 RO1-HD 20889 and 1 RO1-CA 34841 from the National Institutes of Health (to A. C. A. and R. H.). R. C. L. is an American Cancer Society Clinical Fellow.
PY - 1988/10/1
Y1 - 1988/10/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0023804346&partnerID=8YFLogxK
U2 - 10.1016/0165-4608(88)90123-9
DO - 10.1016/0165-4608(88)90123-9
M3 - Article
C2 - 3180012
AN - SCOPUS:0023804346
SN - 0165-4608
VL - 35
SP - 61
EP - 71
JO - Cancer Genetics and Cytogenetics
JF - Cancer Genetics and Cytogenetics
IS - 1
ER -