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.     

单次大剂量放疗对猪胰腺及胰周组织的损伤作用

摘 要：［目的］ 观察不同单次大剂量外放疗对猪胰腺及胰周组织的损伤作用。［方法］ 12头家猪分为7Gy、10Gy、13Gy和16Gy共4组,每组3头进行单次大剂量外放疗,取仰卧位,前后对穿照射,射野面积为10cm×10cm方野,照射后7d处死动物后取材,取受照胰腺组织及胰周组织进行常规切片HE染色,光镜下病理观察。［结果］ 单次大剂量照射后猪胰腺组织的损伤呈明显的剂量依赖性,损伤形式由点状凋亡坏死向大片状坏死转变。［结论］ 提高单次照射剂量在增加胰腺组织损伤的同时也明显增加了胰周组织的损伤。因此,应采用调强适形放疗技术加强对胰周组织的保护。提高单次剂量后引起的胆道损伤应引起注意。     

探讨周围型肺癌MSCT影像学表现与临床组织病理学的相关性研究

目的 旨在探讨周围型肺癌多层螺旋CT(MSCT)影像学表现与临床组织病理学的相关性.方法 回顾性分析2017年12月至2019年1月于我院就诊治疗的68例周围型肺癌患者的临床、影像学资料,以术后病理活检检查结果为标准,分析MSCT检查征象与病理学检查中病灶与组织病理类型之间的关系.结果 不同组织病理类型周围型肺癌患者其...     

生物导弹IgY-RiCin治疗上消化道中晚期恶性肿瘤

目的利用克隆免疫技术探索治疗癌症的新方法.方法从人胃低分化粘液腺癌细胞MGC803中分离出一种癌蛋白P110,并以此蛋白P110为抗原免疫产蛋母鸡,再从免疫过的鸡蛋卵黄中分离出对人低分化粘液腺癌细胞具有选择性识别作用的抗体Igy再与蓖麻毒蛋白的A链偶联成lgyRicinA免疫毒(生物导弹),并对体外培养的癌细胞具有选择性和杀伤能力.结果用Igy-RicinA免疫毒治疗TA小鼠S-78-4肿瘤获得较好的效果,治愈率达84%.临床应用Igy-RicinA治疗上消化道中晚期恶性肿瘤30例,有效率达79.9%,治疗前后肝肾功能及血象检查无异常变化,而且治疗后未发现毒副反应.结论生物导弹Igy-RicinA治疗上消化道肿瘤有一定的作用,因此我们认为Igy-RicinA生物导弹是一种很有发展前途的制剂.     

中国胰腺癌的放射治疗现况

胰腺癌是预后最差的恶性肿瘤之一,发现时多属晚期,因此临床上多进行以减轻症状为目的的姑息治疗。由于失去手术机会,胰腺癌的非手术治疗具有重要意义。目前,以同期放化疗为基础的综合治疗已成为国际上标准的治疗方式。国内对于胰腺癌的放射治疗报道相对较少,为了解当前国内胰腺癌放射治疗的现状,以便确定胰腺癌放射治疗的下一步研究方向,现通过对近年来国内期刊检索资料进行总结分析。     

外照射联合131I-chTNT对小鼠Lewis瘤影响的研究

目的 研究外照射联合¹³¹I-chTNT对荷瘤小鼠肿瘤生长的影响,并观察其在小鼠体内的分布和显像。方法 建立C57小鼠Lewis瘤模型,肿瘤直径达一定大小时随机分组进行实验。测量给药后不同时间肿瘤组织及感兴趣器官的放射性,观察活体显像情况及荷瘤小鼠肿瘤生长延迟效应。结果 联合外照射组肿瘤组织的放射性1、3和5d均高于单药组,组间差异有统计学意义(P值分别为0.018、0.041和0.024),两组中正常组织的放射性差别无统计学意义(P＞0.05)。联合组肿瘤区核素显像比单药组强且持续时间长。肿瘤生长效应实验中单药组、外照射组、联合组的绝对延迟时间为3.1、9.1和13.1d,标准化延迟时间为10d,¹³¹I-chTNT对放射的增益因子为1.08。结论外照射联合¹³¹I-chTNT后可促进其在小鼠体内肿瘤区的浓聚,而对正常组织无影响。联合应用¹³¹I-chTNT可提高外照射对荷瘤小鼠的放射效应。     

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.