摘要
避开化疗诱导多药耐药性的常规方法,建立烷基磷脂类化合物(十六烷基磷酸胆碱,HePC)诱导人上皮性肿瘤细胞系产生交叉耐药。旨在以新的角度认识肿瘤多药耐药性,揭示新的调控机制。利用抑制消减杂交技术,对文库进行克隆分析,在获得的可分析的78个克隆中,27%没有同源基因片段或同源性很低,暂定为“新基因”;14%具有染色体明确定位,认为是化疗敏感肿瘤KB细胞所特有的cDNA片段;19%在人类EST库文库MGC和CGAP中出现,可能是肿瘤细胞特有基因;发现与耐药相关的已知功能基因高达40%。
To avoid the common practice method induced multiresistance.In order to understand the new mulilresist mechanism,the human tumor epitheliacress resistance cells strain KBr that induced by HePC form KB was estab-lished and SSH was used to screen out the differently expressed genes in KB cells.About 78cDNA clone were ob-tained form this library by sequencing.27%genes were not find homologous fragment or lower than homologous frag-ment ,may be new genes.14%genes have chromosome locations,We think that exclusively chemistry resistant tumor cDNA fragment KB cell.19%genes MGC and CGAP appear to human EST library.May be tumor cell have char-acterize by genes.We find more than40%genes are known multiresistance genes The propose is to explore the loss of tumor multiresist genes and find new way to reverse multiresistance.
出处
《生物技术通讯》
CAS
2002年第5期349-352,共4页
Letters in Biotechnology
基金
国家重点基础研究基金项目(G199805120)
