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 conventional method of chemotherapy induced multidrug resistance, the establishment of alkyl phospholipids (Cetyl Phosphocholine, HePC) induced human epithelial tumor cell lines to produce cross-resistance. It aims to recognize the multi-drug resistance of tumor from a new perspective and reveal new regulatory mechanisms. Of the 78 available clones analyzed, 27% did not have homologous gene fragments or had low homology, tentatively designated as “new genes”; 14% had chromosome-specific 19% were found in human EST library MGC and CGAP, which may be tumor cell-specific genes. Up to 40% of the known functional genes related to drug resistance were found.