TRAIL与kallistatin联合表达载体的构建及抗肿瘤活性分析

为研究肿瘤坏死因子相关凋亡诱导配体(TRAIL)与组织激肽释放酶结合蛋白(kallistatin)联合用药的抗肿瘤作用,构建TRAIL与kallistatin双表达的重组质粒pAM-CAG-Kal-IRES-TRAIL,将重组质粒转染A549,LO-2,NCI-H446和Hela细胞,考察其抗肿瘤活性.实验结果表明:构建的双表达载体能同时表达TRAIL与kallistatin,且均能分泌至培养基中;TRAIL与kallistatin联合表达对肿瘤细胞活力的抑制作用明显增强,诱导肿瘤凋亡的作用也明显增强,说明联合表达TRAIL与kallistatin能够增强抗肿瘤活性.     

凋亡抑制蛋白与肿瘤关系的研究

凋亡抑制蛋白(inhibitor of apoptosis proteins,IAPs)可以作为癌症诊断和治疗的靶点,在肿瘤研究方面备受关注,就凋亡抑制蛋白的结构、功能、在肿瘤中的表达与肿瘤的关系等研究进展作一综述,为凋亡抑制蛋白的研究提供信息和思路.     

Surface molecules regulating rolling and adhesion to endothelium of neutrophil granulocytes and MDA-MB-468 breast carcinoma cells and their interaction

The extravasation of leukocytes and tumor cells is a multi-step process with the involvement of various adhesion molecules depending on the three steps rolling, adhesion, and diapedesis. We have developed an in vitro model, by which we investigated the rolling and adhesion of neutrophil granulocytes and MDA-MB-468 human breast carcinoma cells to lung endothelial cells under physiological flow-conditions. We found that norepinephrine had an inhibitory function on the fMLP-promoted adhesion of neutrophil granulocytes due to a down-regulation of β2-integrin. Furthermore, neutrophil granulocytes serve as linking cells for the interaction of the MDA-MB-468 cells with the endothelium, which are both β2-integrin negative, but express the β2-integrin ligand ICAM-1. In addition, we show here that N-cadherin is up-regulated on the endothelial cells and on neutrophil granulocytes in response to fMLP. This up-regulation resulted in a significant increase of adherent MDA-MB-468 cells, which are also N-cadherin positive. Received 3 September 2007; received after revision 17 October 2007; accepted 22 October 2007     

肿瘤患者的心理分析及护理

分析了肿瘤患者心理变化4个阶段的不同表现,并针对此提出相应心理护理的方式。指出加强肿瘤患者的心理分析及护理是保证顺利治愈的重要环节。     

建立人输卵管上皮细胞无血清培养

人输卵管上皮细胞（HOEC）可以体外较长时间无血清培养,DMEM／F12培养液的培养效果优于Ham’sF10,在加有多种因子和胎球蛋白的培养液中,HOEC可贴壁生长,生长能力达到合质量分数15％FCS的对照组的30％～40％,一般可传代2次,最长培养可维持38d,细胞形态与有血清培养差别不大,虽然无血清培养HOEC的生长速度、密度、传代成功率远不及有血清培养,但能抑制成纤维细胞生长,维持较纯的上皮细胞。     

鸭血烯酸对艾氏癌生长的抑制作用

鸭血烯酸是由鸭血清中提取的不饱和脂肪酸．在体外实验中具有使艾氏腹水癌细胞膨胀失活的作用．用于治疗艾氏癌患鼠,可抑制其腹水癌和实体瘤的生长．与环磷酰胺（CPA）或氟脲嘧啶（SFU）相比,鸭血烯酸的毒性较低,疗效较高,约20％～40％被治愈的患鼠,可长期存活．     

颈部肿块细针吸取细胞学诊断

2000—2002年进行颈部肿块细针吸取细胞学检查共600例，有病理组织学证实138例，其中恶性病变66例。淋巴结、甲状腺各占60．10％、23．50％。细胞学阳性158例，占26．33％，可疑恶性32例，占5．33％。和术后病理组织学诊断对照。恶性病变符合率80．30％，良性病变符合率为93．06％，总符合率为86．96％。敏感率(阳性 可疑)淋巴结、甲状腺分别为96．29％和90．00％。本文对假阳性、假阴性病例进行了分析。     

复方癌立消抗肿瘤活性的研究

癌立消为验方，取长白山新鲜中药配制而成，实验用NIH小鼠移植Ehrlieh癌造成实体瘤模型。随机分四组。对照组不给药，阳性对照组给环磷酰胺剂量100mg／kg、癌立消剂量为成人剂量5倍(2．6g／kg)和10倍(5．2g／kg)两组。结果表明：癌立消有明显的抑瘤作用。5倍成人剂量组抑瘤率为43．9％-50．4％，10倍成人剂量组为53．3％-56．3％，而且有统计学意义。     

Inhibitory effect of the adenovirus type 5 E1A protein expressed in the yeast system

The human adenovirus type 5 E1A, a tumor- suppressor gene[1], codes for two major related proteins of 243 amino acids (12S) and 289 amino acids (13S) by al-ternative splicing in two exons[2]. Studies have been shown that E1A can regulate expression of many genes and cell cycle[3]. Both in vitro and in vivo experiments indicated that E1A could induce tumor cells differentia-tion, convert tumor cells into an epithelial phenotype, in-hibit tumor cell growth and metastasis and strongly en-ha…     

Inhibitory effect of the adenovirus type 5 E1A protein expressed in the yeast system of the human tumor cell growth

Adenovirus 5 type E1A as a tumor suppressor gene can inhibit tumor growth and enhance the censitivity of chemotherapy and radiotherapy.E1A have the ability to integrate into the host genome,resulting in long-time expres-sion that induces Rb gene inactivation and animal cells im-mortalization.This prompted us to select the E1A protein for treatment of cancer in order to overcome the limitations of E1A gene therapy.Thus,we firstly comstructed E1A eu-caryotic expression vector (pPIC9/E1A),transformated the pichia pastoris yeast cells(GS115) and screened the high-expressing recombinant strains.The positive yeast strains were cultured in the shake flask,and induced for 3d.The crude E1A protein was purified using two steps of col-umu chromatography on HiTrap Q and HiTrap SP.The pu-rified E1A protein was identified by SDS-PAGE and Western blot.E1A protein was mostly located at cellular unclear when Cheriot delivered E1A protein into cells.The analysis in vitro indicated that the E1A protein arrested LN686 cell cycle at G2/M phase,and significantly inhibited the growth of LN686 tumor cells.The current studies firstly provided an experimental basis to further develop E1A protein for tumor treatment.