International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 110 - GENOMICS-ARRAY DISPLAYS THE DIFFERENCES IN MECHANISM OF BENZENE LEUKEMOGENICITY BETWEEN ONE IN P53-DEFICIENCY AND THE OTHER IN THE WILD-TYPE C57BL/6 MICE

MD Yoko Hirabayashi
National Institute of Health Sciences
1-18-1, Kamiyohga, Setagayaku
Tokyo
158-8501
Japan

Co-Authors: 1)Yoon B-I, 1)Kawasaki Y, 1)Kodama Y, 2) Aizawa S-i, 1)Kaneko T, 1)Kanno J, 1)Inoue T
Institutions: 1)Div. of Cell. & Molecul. Toxicol, NIHS, 2) Inst. of Dev. Biol, Kumamoto Med. School,

Two inconsistent phenotypes after benzene exposure, i.e., the suppression of BM cells (Irons, 1979) and the increase of cycling fraction in CFUs (Cronkite & Inoue, 1982), make understanding the mechanism of leukemogenicity problematical. In the present study, a newly developed measure for the cell-cycle of CFUs, the BUUV method, disclosed not only the underlining background of the inconsistency but also defined the separate mechanism of leukemogenicity in wild type mice and p53 deficiency. In p53+/+ mice, p53 dependent-oscillational suppression in marrow cellularity was seen during/after benzene exposure, with concurrent suppression/expression of p21. This oscillation was not observed in p53 deficient mice. cDNA micro-array examined along with the benzene exposure protocol showed a compatible variety of gene expressions pertinent to the cell cycle, including cyclin-dependent kinases. Taken together, our present data suggest that in the case of wild type mice, the p53 dependent-oscillational changes in cell-cycle may not induce substantial genotoxic leukemogenesis but rather contribute to an epigenetic one whereas in p53 deficient mice, un-repaired DNA damages under the p53 deficiency may contribute to induce a genotoxic leukemogenesis. In reverse, cDNA micro-array differentiates the difference of expression profiles between in the cases with or without p53 gene expression.


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