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  • Title: Resistance to 1-Beta-d-arabinofuranosylcytosine and hypersensitivity to bleomycin in ataxia-telangiectasia B-lymphoblastoid cell-lines.
    Author: Li M, Shiraishi Y.
    Journal: Int J Oncol; 1994 Jun; 4(6):1173-81. PubMed ID: 21567034.
    Abstract:
    Three ataxia telangiectasia (AT) B-lymphoblastoid cell lines (B-LCLs) were examined for the chromosome aberrations induced by a DNA replication and repair inhibitor, 1-beta-D-arabinofuranosylcytosine (ara-C), and the effects of ara-C on the frequencies of chromosome aberrations caused by bleomycin (BLM). All these AT cell lines exhibited resistance to ara-C compared with normal and Bloom syndrome (BS) cells. In contrast with normal and BS cells, ara-C did not enhance chromosome aberrations produced by BLM in AT cells, although these cells showed hypersensitivity to BLM. After treatment with 1 X 10(-5) M ara-C for 24 h, total frequencies of chromosome aberrations in AT cells were 0.095-0.115/cell, which is about 6 times lower than those in normal (0.625/cell) and BS cells (0.775/cell). Following combination treatment with tetrahydrouridine (THU) and ara-C, we found that the frequencies of chromosome aberrations in AT B-LCLs were greatly increased compared with treatment with ara-C alone. Furthermore, when AT cells were pretreated with THU in combination with ara-C, then treated with BLM, a great synergistic enhancement of chromosome aberrations was observed. Because THU is an exclusive inhibitor of cytidine deaminase, these results strongly indicate that in AT B-LCLs there could be overproduction of cytidine Jeaminase, which is responsible for ara-C resistance. On the other hand, combination of THU and deoxycytidine (dCyd) significantly reduced chromosome aberrations induced by BLM in AT cells, although dCyd alone had no effect on bleomycin-induced chromosome aberrations. Break point distributions on chromosome bands following treatment with BLM or ara-C plus THU, alone or in combination, were examined and are discussed.
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