Abstract
Point mutation of N-ras oncogene at codons 12, 13 and 61 was studied in the bone marrow cells of patients with typical aplastic anemia using the polymerase chain reaction method for DNA amplification and dot blot hybridization to synthetic oligonucleotide probes. Point mutation was observed in none of the 15 patients studied. These findings indicate either that the pathogenesis of typical aplastic anemia is different from that of preleukemic states of myelodysplastic syndrome or acute leukemia in clonal evolution, or that the overlapping area sharing a common pathogenesis is much smaller than was presumed.
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