局部复发直肠癌放射治疗

局部复发是直肠癌,尤其是Ⅱ/Ⅲ期直肠癌手术治疗失败的主要原因,且术后复发病例预后差。20世纪70年代开始局部进展期直肠癌手术前后辅助放化疗的相关研究。大量临床试验结果显示,术后或术前辅助性放化疗较单纯手术可降低局部复发率、提高保肛率和存活率,已经成为I类循证医学证据,作为局部进展期直肠癌的标准治疗方案。而术后局部复发的直肠癌放化疗,目前尚未取得较高级别的循证医学证据。美国国家癌症综合网络（NCCN）指南建议对复发直肠癌病人应该采用多学科合作的综合治疗方案。孤立的盆腔或吻合口复发,如果之前未接受过全量放疗,最适合的处理就是行术前放疗,同期化疗。有条件的医疗机构,可考虑行术前新辅助放化疗+手术切除+术中放疗。     

高强度聚焦超声联合放射治疗对猪胰腺及超声声窗组织与脏器损伤作用的观察研究

目的观察高强度聚焦超声(HIFU)联合放射治疗对猪胰腺目标的治疗作用及腹部声窗上组织和脏器的损伤情况。方法实验猪共12头,每组3头,分为对照组、HIFU组、放疗组和联合治疗组(HIFU与放疗)。放射治疗及HIFU治疗均参照临床治疗参数进行,对大体标本根据不同损伤程度评为0～3分,组织病理学根据细胞变性坏死情况分为0～4分进行评分,根据损伤及评分情况评价胰腺目标及超声和放射治疗通路上组织、器官的损伤情况。结果 (1)胰腺损伤病理观察评分结果:联合治疗组评分值高于HIFU组,两组评分结果比较差异有统计意义(t=4.161,P=0.003)。(2)胃壁损伤病理观察评分结果:联合治疗组评分值略高于HIFU组及放疗组,但评分结果比较差异无统计学意义。(3)肠壁损伤病理观察评分结果:联合治疗组及放疗组评分值均高于HIFU组,评分结果比较差异有统计学意义(t=2.827,P=0.022),联合治疗组与放疗组评分结果比较差异无统计学意义。各组实验动物耐受性好,未发生严重并发症。结论与HIFU组及放疗组相比,对活体猪行HIFU联合放射治疗增加了在体胰腺组织的治疗性损伤作用;但HIFU联合放疗治疗未增加HIFU对非目标区组织的损伤,主要损伤表现与放射治疗有关。     

第四届亚洲放疗联盟学术会议圆满结束

亚洲放射肿瘤联盟(FARO)成立于2014年,是由亚洲国家参与的国际性、专业性、学术性、非营利性社会组织。现共有14个成员国,原有中国、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、巴基斯坦共12个国家,本次会议通过缅甸及蒙古国成为新成员。FARO旨在加强亚洲地区放射肿瘤学组织的合作交流,自2016年起每年举办1次会议,同时开展相关教育培训、加强研究合作、制订亚洲共识。     

炎性乳腺癌新辅助放疗四例临床分析并文献复习

目的通过4例炎性乳腺癌新辅助放疗病例及文献复习，分析探讨炎性乳腺癌新辅助放疗的可行性。 方法回顾性分析4例临床分期为T_4dN_1~3M₀的炎性乳腺癌患者，新辅助全身治疗失败后加用新辅助放疗，观察其疗效，并回顾分析相关文献。 结果4例炎性乳腺癌患者新辅助放疗后均获得临床缓解，成功进行乳腺癌改良根治术。术后无严重并发症，手术切口愈合良好，无坏死。1例患者术后病理完全缓解，3例部分缓解。中位随访时间26个月（18~103个月），1例胸壁复发，2例肺、纵隔淋巴结转移，1例无复发转移。1例死亡（肺转移）。 结论精确放射治疗技术对新辅助全身治疗失败的炎性乳腺癌患者进行新辅助放疗，安全有效。     

巨块型NSCLC质子部分立体定向消融推量放疗的剂量学优势

目的 探索肿瘤长径>8 cm的巨块非小细胞肺癌（NSCLC）放疗中质子部分立体定向消融推量放疗（P‐SABR）的剂量学优势。方法 收集既往应用光子P‐SABR治疗的9例巨块NSCLC的定位影像。在光子肿瘤推量靶区（光子GTVb）基础上逐步外扩,直到重要危及器官受量达3.0 Gy/次时停止,形成质子肿瘤推量靶区（质子GTVb）,质子GTV、CTV范围同光子,分别制订光子固定野调强放疗（光子FF‐IMRT）、光子容积调强弧形治疗（光子VMAT）、质子调强放疗（IMPT）计划。对比不同治疗技术的剂量学参数。结果 光子GTVb和质子GTVb占GTV体积比分别为25.4%±13.4%和69.7%±30.0%（P<0.001）。光子IMRT、光子VMAT、IMPT的CTV平均剂量分别为（76.1±4.9）Gy、（78.2±3.6）Gy、（84.7±4.9）Gy,生物有效剂量（BED）≥90 Gy所包含肿瘤占GTV体积的百分比分别为70.7%±21.7%、76.8%±22.1%、97.9%±4.0%,质子较光子P‐SABR计划显著提高了靶区剂量及BED（P<0.05）。质子较光子计划还降低了危及器官受量,其中光子FF‐IMRT、光子VMAT和IMPT的双肺V_{5 Gy}分别为49.2%±22.0%、56.8%±19.0%和16.1%±6.3%（P<0.001）。结论 质子P‐SABR较光子可在降低危及器官受量情况下,扩大肿瘤推量靶区范围并提高肿瘤内BED,有望进一步提高巨块NSCLC的局部控制率。     

食管癌放射治疗的现在及未来

<正>食管癌是较常见的消化道恶性肿瘤之一,其发病具有明显的地区性,中国食管癌发病率居世界之首,是低发地区西部非洲的20倍[1],据估算全世界约53.8%的食管癌患者在中国[2]。全世界食管     

放射抗拒性食管癌细胞系的建立及基因表达差异分析

目的观察食管癌细胞经射线反复照射后放射敏感性的变化，应用基因芯片技术分析放射抗拒性食管癌细胞基因表达变化。方法食管鳞状细胞癌细胞株TE13经反复γ射线照射（累积剂量120Cy），逐步筛选出具有放射抗拒性的细胞TE13R120。相差显微镜下观察TE13及TE13R120的形态学差异；应用细胞克隆形成实验，验证TE13及TE13R120两种细胞的不同放射敏感性，用流式细胞术检测它们的细胞周期分布特征；基因芯片分析两种细胞基因表达差异。结果TE13R120的细胞群体倍增时间为39．93h，长于亲代TE13（33．94h）。TE13及TE13R120的放射敏感性明显不同（仇值分别为1．63和2．85Gy，SF2值分别为0．55和0．64，Dq值分别为1．38和1．15Gy，n值分别为2．33和1．49）。两种细胞经4Gy放射线照射后，出现不同的细胞周期分布改变，12～48h TE13R120细胞周期变化不明显，而其亲代细胞TE13发生明显G1期阻滞。应用DNA芯片对2159个基因进行了筛选，TE13R120与TE13相比，上调基因96个，下调基因80个。结论新的食管癌细胞系TE13R120比其亲本对射线更加抗拒，并且在基因水平上发生明显变化。4Gy照射后12～48hTE13R120细胞周期变化不明显，而其亲代细胞TE13发生明显G1期阻滞。     

放射治疗食管癌CT分期的研究

目前使用的国际抗癌联盟 (UICC)和美国癌症联合会 (AJCC)食管癌TNM分期标准是以手术后的病理诊断为基础的 ,而对于像放射治疗这样的非手术的食管癌患者 ,因无实体标本则不能进行准确的分期。目前国内外有关放射治疗食管癌的文章多根据影像学资料套用UICC和AJCC食管癌TNM分期标准 ,但在套用时无统一标准 ,个人主观性很大 ,存在着很大差异 ,影响分期的一致性和各研究之间的可比性。CT在我国已基本普及 ,对于中晚期食管癌CT能显示病灶与周围结构的关系 ,观察增大的淋巴结 ,发现远处脏器转移 ,因此对食管癌分期、治疗手段的选择和预…     

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.