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1、上海第二醫(yī)科大學(xué)博士學(xué)位論文Apilotstudyonmechanismbasedtargetedtherapyft(821)leukemia姓名:周光飚申請(qǐng)學(xué)位級(jí)別:博士專業(yè):內(nèi)科學(xué)(血液病學(xué))指導(dǎo)教師:王振義2003.5.1上海第二醫(yī)科大學(xué)博士研究生畢業(yè)論史種效應(yīng)呈劑量一時(shí)間依賴性。SIHl0可引起Kasumi1細(xì)胞線粒體跨膜電位的崩解、caspases的活化,而且可引起AMLI—ETO蛋白的裂解。給腹水瘤NOD/SCID小鼠腹腔注
2、射75、15mg/(kgd)的SIHl016至28天,可誘導(dǎo)腹水Kasumi一1細(xì)胞凋亡,減慢荷瘤小鼠體重的增加,延長(zhǎng)其生存期(比對(duì)照組分別延長(zhǎng)32%與44%),使NOD/SCID小鼠體內(nèi)白血病細(xì)胞的器官組織浸潤(rùn)程度減輕,并引起肝臟浸潤(rùn)部位的大片白血病細(xì)胞原位凋亡,而未見(jiàn)明顯副作用。結(jié)果表明,SIHl0降解AMLlETO融合蛋白誘導(dǎo)t(8:21)白血病細(xì)胞凋亡,改善荷瘤小鼠預(yù)后,可能是人類t(8:21)白血病靶向治療的候選藥物,具有潛在
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