To investigate the specific chromosomal abnormalities and role on oncogenes in human acute leukemia, bone marrow cells from ten cases of acute leukemia patients were cultured and karyotyped after G-banding. DNA in situ hybridization was also
performed
on the same samples with K-ras, erb-B2, mos and p53 oncogenes. The most characteristics of chromosome abnormalities were marker chromosomes, deletion types of (1) (q26), (2) (q25), (7) (q25), 8(q26) (16) (q24) and t(3;10) (q12;q11) in AML, while
deletion types of (1) (q28), (1) (p11), (9) (q34) and t(9;22) (q34;q12) were found in ALL. It was found that three oncogenes (erb-B2, mos, p53) except K-ras were activated with translocation in both subtype leukemia by DNA in situ hybridization.
It
was
obscure that chromosome aberrations and activation of oncogenes were not corelated by individuals. It is presumed that acute leukemia-related antioncogenes are located on the chromosome 1 and 2 and direct activating gene causing acute leukemia in
oncogenesis is located on the chromosome 9. An activation of erb-B2, mos and p53 is related to the secondary effect on oncogenesis in acute leukemia.
|