[Abnormalities of the p53, N-ras, DCC and FLT-3 genes in myelodysplastic syndromes].
The molecular mechanism of carcinogenesis is a multistep process that is characterized by both activation of oncogenes and inactivation of tumor suppressor genes. In the present study, mutations of N-ras, p53 and FMS-like tyrosine kinase 3 (FLT-3) genes and loss of expression of the deleted in colorectal carcinoma (DCC) gene were analyzed in 59 patients with myelodysplastic syndromes (MDS). Mutations of N-ras, p53, and FLT-3 genes were detected in 7, 7, 1 of the 59 patients with MDS, respectively. Loss of DCC expression was detected in 16 patients. Type of MDS patients with N-ras mutation were all refractory anemia with excess of blasts in transformation (RAEB-T). Abnormalities of p53 and DCC genes were significantly associated with survival time (p< 0.02, p< 0.004, respectively).
Nakamura
K
K
Department of 3rd Internal Medicine, Nippon Medical School, Tokyo, Japan.
Inokuchi
K
K
Dan
K
K
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D016163:Genes, DCC / Q000235:genetics; D016158:Genes, p53 / Q000235:genetics; D011905:Genes, ras / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009190:Myelodysplastic Syndromes / Q000235:genetics*; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics*; D051941:fms-Like Tyrosine Kinase 3
D011518:Proto-Oncogene Proteins; C497970:FLT3 protein, human; D020794:Receptor Protein-Tyrosine Kinases; D051941:fms-Like Tyrosine Kinase 3