作者: P. DeFeudis , M. D'Incalci , M. Broggini
DOI: 10.1007/BF01321023
关键词: Tallimustine 、 Apoptosis 、 Fusion protein 、 Biology 、 Cancer research 、 Fusion gene 、 Cisplatin 、 DNA fragmentation 、 K562 cells 、 Cell culture
摘要: Chronic myeloid leukaemia (CML) cell lines expressing the bcr-abl fusion gene are resistant to drug-induced apoptosis. Using a human CML line (EM2), we investigated effects of cisplatinum (DDP), Doxorubicin and Tallimustine on level p210, product hybrid gene, induction DDP exposure this resulted in decrease p210 levels with concomitant activation At all concentrations tested, neither nor were able induce DNA fragmentation reduce protein p210. The reduction induced by also observed at mRNA as RT-PCR, suggesting that, least part, was result transcription gene. DDP-induced levels, EM2 cells but not another (K562) which overexpresses In K562 bcr-abl, although decreased, remained well detectable after treatment. Data indicate that it may be possible investigate compounds contrast resistance DNA-damage apoptosis lines.