目的：研究卵巢癌组织中表皮生长因子受体（epidermal growth factor receptor，EGFR）基因突变的情况，为卵巢癌的靶向治疗提供实验依据。方法：收集南昌大学第二附属医院与江西省肿瘤医院70例卵巢癌组织标本，采用多聚酶链式反应（polymerase chain reaction，PCR）及多聚酶链式反应-限制性内切酶片段长度多态性（PCRrestriction fragment length polymorphism，PCRRFLP）分别检测卵巢癌组织EGFR基因是否有第19外显子的缺失及第21外显子的L858R点突变。结果：在70例卵巢癌组织中，PCR未检测到EGFR基因第19外显子缺失突变，PCRRFLP未检测到第21外显子的L858R点突变。结论：卵巢癌组织EGFR基因中未检测到第19外显子缺失突变和第21外显子的L858R点突变。

Objective:To investigate the antitumor activity of cytokineinduced killer cells (CIKs) against cervical cancer cell lines, CasKi and HeLa in vitro and in vivo. Methods: The CIKs were induced from peripheral blood mononuclear cells (PBMCs) of patients with cervical cancer using an improved method, which only used IL2 and antiCD3 antibody, without IFNγ; CIKs were sorted using FACS. The levels of IFNγ, IL2 and TNFα in culture supernatants of CIKs were determined by ELISA. The antitumor activities of CIKs against CasKi and HeLa cells were determined by LDH assay. The nude mouse xenograft models of cervical cancer cell lines, CasKi or HeLa cells, were established, and 1×106 or 1×107 CIKs were administered intravenously once a week for three weeks, then the tumor volumes and weights were measured.Results: CIKs were successfully induced from PBMCs of cervical cancer patients by IL2 and antiCD3 antibody, with CD3+CD56+ cells greatly expanded. CIKs produced significant amounts of IFNγ and TNFα, but few IL2, after PHA stimulation. CIKs dosedependently killed CasKi and Hela cells with a maximum killing rate reaching 43% and 46%, respectively. In addition, the in vivo antitumor experiments demonstrated that CIKs remarkably inhibited the growth of subcutaneous tumors in nude mice (P<0.01). Conclusion: The improved CIKs expansion method used in our study is feasible and the resultant CIKs have remarkable cytotoxicity against Caski and HeLa cells both in vivo and in vitro.

江西省教育厅科学技术研究项目（No.GJJ09120）