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国家自然科学基金(30670619)

作品数:4 被引量:23H指数:3
相关作者:高献书王雅棣杨俊泉王小虎李海滨更多>>
相关机构:北京大学第一医院辽宁省肿瘤医院邯郸市中心医院更多>>
发文基金:国家自然科学基金更多>>
相关领域:医药卫生生物学更多>>

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甘氨双唑钠胸段食管鳞癌放射增敏作用——Ⅲ期多中心随机对照研究被引量:15
2012年
目的评价放射增敏剂甘氨双唑钠在胸段食管鳞癌放疗中的疗效和不良反应。方法2008-2009年间采用多中心、随机、双盲方法对不耐受或拒绝同期放化疗Ⅱa~Ⅲ期和仅锁骨上淋巴结转移Ⅳ期(第6版MCC分期)患者进行临床试验,经病理证实的胸段食管鳞癌66例患者随机分为A、B组。A组用甘氨双唑钠800mg/m。溶于100ml生理盐水30min内静脉滴注后30~60min完成放疗,B组用安慰剂放疗。放疗总剂量66Gy(1.8~2.0Gy/次,5次/周,6.6~7.2周完成)。A组剔除1例,B组剔除3例,可分析病例两组各31例。结果随访率为97%。A、B组患者近期总有效率分别为93.5%、67.7%(χ^2=6.61,P=0.01),2年总生存率,无进展生存率,肿瘤特异生存率分别为39.9%、29.9%,30.1%、27.9%,43.1%、26.8%(χ2=0.62、0.02、0.30,P=0.433、0.878、0.586)。所有患者耐受良好,未发现严重不良反应。结论研究显示,甘氨双唑钠作为放射增敏剂,在近期疗效上两组患者差异有统计学意义,且患者耐受性良好。本次随访期内,生存率未见明显改善。
秦尚彬王雅棣杨俊泉王小虎李海滨杨志勇于洪李雪迎高献书
关键词:甘氨双唑钠放射增敏剂食管肿瘤
Differential gene expression profiles of DNA repair genes in esophageal cancer cells after X-ray irradiation被引量:3
2010年
Bckground and Objective: Various factors affect the radioresistance of tumor cells, with unknown molecular mechanism(s). Many genes have been found to associate with the radioresistance of tumor cells, however, the precise mechanism of these genes have not been elucidated. This paper was to analyze the differential expressions of DNA repair genes in esophageal carcinoma cells at different time after X-ray irradiation, and to investigate the role of these DNA repair genes in radiation resistance. Methods: Esophageal cancer parental cells Seg-1 were treated with continuous 2 Gy of fractionated irradiation until the total dose reached 60 Gy to establish the radioresistant cell line Seg-1R. Total RNA was extracted from each cell line at 0, 8, and 24 h after irradiation. Illumine Human-6 V3 microarray was used to identify differentially expressed genes between parental and radioresistant cells. Ten genes involved in DNA repair were obtained and their expressions at different time points after irradiation were analyzed by Gene Ontology analysis. Results: Ten DNA repair associated genes were found to be differentially expressed. Three of these genes, SLK, HMGB1, and PMS1, were not only differentially expressed between parental and radioresistant cell lines, but also expressed differently at different time points after irradiation in the same cell line. Conclusions: PMS1 may be an important factor involved in the mechanism of radioresistance of esophageal carcinoma cells.
Hai ZhangXian-Shu GaoJing ZhaoWei XiongMin ZhangHong-Zhen LiDe-Min ZhouXin JinDan-Shen Zhang
关键词:DNA修复基因食管癌细胞X射线照射基因差异总RNA提取
Identification of differentially expressed genes related to radioresistance of human esophageal cancer cells被引量:5
2010年
Background and Objective: Radioresistant cells in esophageal cancer is one of the important reasons for the local failure of radiotherapy. In recent years, some researchers used gene chip technology to screen the differentially expressed genes between parental and radioresistant human esophageal cancer cells. But there were some problems in these studies, for example comparing cells at only one time interval, and genetic background not matching. In this study, we selected 3 different pairs of parental and radioresistant human esophageal cancer cells, and compared the gene expression profiles by cDNA microarray at 3 time intervals to identify and analyze the differentially expressed genes between parental and radioresistant human esophageal cancer cells. Methods: We compared the gene expression profiles between parental cells (TE13, Seg-1, Kyse170) and radioresistant cells (TE13R, Seg-1R, Kyse170R) before, and at 8 h and 24 h after irradiation with a cDNA microarray consisting of 48 000 genes (Human Genome). We identified differentially expressed genes by Pathway and GO analyses, and verified the differentially expressed genes LEF1 and CTNNB1 by RT-PCR. Results: A total of 460, 451, and 397 differentially expressed genes were found before, and at 8 h and 24 h after irradiation. After Pathway and GO analyses, 14 differentially expressed genes, participating in cell growth, apoptosis, cell cycle regulation, gene repair and signal transmission, were selected to further research. LEF1 and CTNNB1 were verified by RT-PCR, and the results were consistent with those of cDNA microarray. Conclusions: The WNT signal pathway may be an important pathway participating in the formation of radioresistance of esophageal cancer cells. LEF1 and CTNNB1 may be the important genes causing the esophageal cancer cell radioresistance.
Hong-Zhen LiXian-Shu GaoWei XiongJing ZhaoHai ZhangDe-Min Zhou
关键词:食管癌细胞CDNA微阵列基因芯片技术
放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤
2009年
目的观察放射线联合p53基因及内皮抑素治疗C57BL/6小鼠前列腺癌皮下移植瘤的效果,并初步探讨其作用机制。方法建立C57BL/6小鼠前列腺癌皮下移植瘤模型。随机分成5组:空白组(A)、放射组(B)、放射线联合p53基因组(c)、放射线联合内皮抑素组(D)及放射线联合p53基因和内皮抑素组(E)。第1天c、E组瘤内注射p53基因腺病毒(1×10^10vp),第1-14天D、E组每日1次腹腔注射内皮抑素(1.5mg/kg)。第4天B、c、D、E组小鼠肿瘤区单次照射(6MVX线DT15Gy)。每日测量肿瘤体积;检测各组肿瘤标本P53、Ki67及血管内皮生长因子(VEGF)的表达及微血管密度值(MVD)。结果4个治疗组的肿瘤生长速度均低于空白组(P=0.000),其中E组生长最慢(P〈0.05)。免疫组织化学结果:4个治疗组P53的表达均明显低于空白组(P=0.000);4个治疗组Ki67的表达均高于空白组,但变化趋势不同:B、c组Ki67的表达值接近,均随时间的推移而逐渐升高(P=0.000),D、E组的表达则呈现波动性;第5天时E组VEGF的表达最低(P〈0.05);肿瘤生长过程中各组MVD值均持续升高,c、D、E3组MVD值在各时间均高于空白组(P〈0.05)。结论放射线联合p53基因及内皮抑素的抑瘤效果优于单独放射治疗及放射线联合p53基因或内皮抑素。三者均有自己的作用机制,但相互之间可以互相影响。
张敏任军徐博高献书何志嵩何晓明张明刘朝兴何新勇曹光明张绍龙
关键词:前列腺癌内皮抑素
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