信息动态

亚洲放射肿瘤联盟(Federation of Asian Organizations for Radiation Oncology,FARO)由日本群马大学教授中野隆史教授、京都大学平冈真宽教授、北京大学高献书教授、印度Ramesh Bbilimagga教授及印度尼西亚Soehartati Gondhowiardjo教授共同发起,最初由11个亚洲国家(中国、孟加拉国、印度、印度尼西亚、日本、韩国、马来西亚、菲律宾、新加坡、斯里兰卡、泰国)的学术组织参与商议.中方委员为李哗雄教授、高献书教授、易俊林教授.会议选举出5人组成的常委会,负责亚洲放疗联盟的组织及运营工作,其中包括中方的高献书教授.2015年5月,第一届FARO常委会在日本京都召开.     

荷瘤小鼠静脉注射洛铂和顺铂后药物浓度的变化规律

目的研究洛铂和顺铂在小鼠血浆、肾脏和肿瘤内的药物浓度随时间变化的规律,为放疗增敏提供实验数据。方法 70只C57BL/6近交系Lewis肺癌荷瘤小鼠随机分组,按10mg药物/kg体重经尾静脉分别给小鼠注射药物（洛铂或顺铂）,给药后在0.5、2、4、24、48、72、96 h分别将小鼠处死获取血液和组织标本（肿瘤和肾脏）,应用ICP-MS方法测定标本铂含量。结果洛铂和顺铂的血浆药时曲线均符合三室模型,半衰期分别为51.139h和35.583h,洛铂在血浆中的清除速率大于顺铂[0.532L/（h.kg）对0.192 L/（h·kg）];洛铂和顺铂在肿瘤组织的浓度均在给药后迅速达到最大[（2.79±0.35）μg/g对（4.78±1.11）μg/g],然后迅速下降,在4 h后分别降至0.99±0.21μg/g和3.39±0.55μg/g,在96 h肿瘤中仍有药物存在,浓度分别为0.23±0.05μg/g和1.41±0.71μg/g。肿瘤药物浓度与血浆药物浓度呈对数相关,Rsq分别为0.948和0.837。结论洛铂和顺铂在小鼠体内静脉给药后半衰期长,肿瘤内药物浓度在给药后很快达到最大,在4 h降至平台期,96 h仍有药物存在,顺铂在肿瘤内的浓度高于洛铂;洛铂在小鼠体内的清除速率快于顺铂;可以通过检测血浆中的洛铂和顺铂浓度来估算肿瘤内的药物浓度。     

前列腺癌术后中等分割放射治疗I期临床研究

目的 评价前列腺癌术后中等分割照射的急性不良反应。方法 选取2017年2月至8月,本院20例前列腺癌术后患者入组。中等分割处方剂量为盆腔45 Gy/25次,1.8 Gy/次;前列腺床62.75 Gy/25次,2.51 Gy/次。不良反应的评价采用北美放射肿瘤协作组（RTOG）急性不良反应评价标准和常见不良事件评价标准（CTCAE）4.0。结果 中位随访时间7.5个月。1例（5%）患者出现了2级急性胃肠反应;2例（10%）患者出现了2级急性泌尿反应。2例（10%）患者放射治疗期间出现了2级尿失禁,放疗后1个月恢复至0级或1级。结论 与既往常规分割照射文献相比,前列腺癌术后中等分割照射模式（2.51 Gy/次×25次）没有明显增加患者急性胃肠、泌尿系统不良反应。近期随访结果显示,没有增加患者尿失禁风险。     

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

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

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

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

食管癌连续7天常规分割加速放射治疗的远期疗效分析

目的连续7d常规分割加速放射治疗方案和后程加速超分割放射治疗方案治疗食管癌的疗效比较。方法57例食管鳞癌患者随机分为两组，连续7d常规分割加速放射治疗组（连续组）29例和后程加速超分割放射治疗组（后超组）28例。连续组治疗方法1次，d，2Gy／次，7d，周，吸收剂量60Gy，30次，30d；后超组前半程为常规分割（5次，周，2Gy／次），照射至30Gy时改加速超分割（2次，d，1．5Gy／次，5d，周），吸收剂量60Gy，共35次，33～35d。结果连续组和后超组1年、2年、3年总生存率分别为62．07％、37．93％、25．60％和64．29％、35．71％、25．00％。1年、2年、3年局部控制率连续组和后超组分别为82．93％、70．59％、52．94％和70．38％、45．95％、40．84％，3年疾病特异性生存率连续组为28．72％，后超组为25．00％。两组间晚期反应差异未见统计学意义。结论连续组3年生存率与后超组相当，局部复发、未控和转移仍是食管癌放射治疗失败的主要原因。     

食管癌后程加速放射治疗前瞻性随机研究

关于食管癌患者后程加速放射治疗的近期疗效及３年生存率已报道过,现就全部病例随访５年（随访率１００％）的生存及局部控制情况简报如下。１　材料与方法经病理证实为鳞癌的１００例食管癌患者,均为首程放射治疗。男７４例,女２６例,平均年龄６０岁。颈段癌４例,胸上段癌３５例,胸中段癌５６例,胸下段癌５例。平均病变长度７１ｃｍ。随机分为２个组,常规组５０例,后程加速超分割组（后加速组）５０例。照射方法：采用４ＭＶ－Ｘ线或１０ＭＶ－Ｘ线照射,常规组每日１次,每次１８０～２００ｃＧｙ,５次／周,总量６０００ｃＧ…     

食管癌再程放疗的疗效观察

对食管癌放疗后局部复发或未控行再程放疗的评价不一。我科自1971年2月至1989年9月,收治资料完整的食管癌放疗后复发或未控行再程放疗者47例(治疗组),与同期未行再程放疗者41例(对照组),进行对比分析,试图提出对再程放疗的看法。     

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

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.