脑胶质瘤术后放疗疗效及预后影响因素分析

目的探讨脑胶质瘤术后放疗疗效及预后影响的相关性因素。方法将脑胶质瘤患者性别、年龄、切除程度、级别、手术放疗时间、放疗方式、肿瘤直径、术前KPS评分、术前水肿情况、放疗剂量纳入研究,计算上述指标与胶质瘤术后放疗疗效的相关性。结果患者治疗后1年、2年、3年的生存率分别为82．9％（126／152）、57．9％（88／152）、32．2％（49／152）。单因素分析结果显示,患者年龄、切除程度、级别、手术放疗时间、术前KPS评分为影响脑胶质瘤术后放疗疗效的相关因素。COX多因素分析显示,年龄、KPS评分、手术切除程度对脑胶质瘤患者预后具有影响。结论手术联合放疗对脑胶质瘤具有明显的手术疗效,年龄、KPS评分、手术切除程度对脑胶质瘤患者预后具有影响。     

脑胶质瘤的显微手术治疗

目的 探讨显微手术治疗脑胶质瘤的效果.方法 回顾性分析2000年至2004年80例脑胶质瘤患者接受显微手术的临床资料.结果 62例行显微镜下全切除,18例行大部分或部分切除,术后常规行放疗及化疗.术后随访,Ⅰ～Ⅱ级星型细胞瘤术后3年生存率达74.29%.Ⅲ～Ⅳ级星型细胞瘤3年生存率为15.35%.结论 显微手术治疗脑胶质瘤,损伤小,全切除率高,临床疗效好,可提高患者的生存时间.     

脑胶质瘤干细胞研究进展

脑胶质瘤是常见的脑原发恶性肿瘤,其治疗主要依据WHO分级;手术切除为首选,术后放疗及放化疗是提高脑胶质瘤生存期的重要手段.低分级脑胶质瘤的治疗效果较好,生存期较长;而高分级患者治疗后的生存期只能以月来描述.脑胶质瘤治疗失败的主要原因是局部复发,而导致复发的重要原因是胶质瘤干细胞未得到有效控制.因此,脑胶质瘤干细胞的鉴别及生物学特性的研究成为近年来国内外学者关注的热点,笔者综述脑胶质瘤干细胞的研究进展.     

高级别脑胶质瘤放疗剂量分割研究现状及进展

高级别脑胶质瘤恶性度高,手术加术后常规放疗及化疗综合治疗是目前标准治疗方案,但疗效仍未见明显改善。研究显示高级别脑胶质瘤对放疗敏感度差,这就需要探索不同放疗分割模式的获益可能,为改善高级别脑胶质瘤患者的预后,近年来不少学者在放射治疗分割方式方面做了大量研究。本文就脑胶质瘤放疗剂量分割现状及其疗效作一总结。     

70例脑胶质瘤术后放疗生存率分析

脑胶质瘤来源于神经胶质，是最常见的中枢神经系统肿瘤，占颅内肿瘤的40％。目前对脑胶质瘤的治疗仍以手术为主，但无法提高生存率。近年手术后的配合放疗有些报道。现将我院1989年8月至1991年8月脑胶质瘤术后放疗资料小结如下。1资料临床资料资料来自我科经病理确诊的脑胶质瘤     

39例高分级脑胶质瘤术后放疗疗效及预后因素分析

高分级脑胶质瘤(HGG)占原发脑肿瘤的35%～45%~([1]).因其多向周围浸润,手术难以彻底切除,术后放疗是目前的标准治疗.笔者回顾分析2004年9月至2007年7月在本院放疗的39例HGG患者手术和术后放疗疗效,以及影响预后的因素.     

放疗合并颈动脉灌注综合治疗术后脑胶质瘤

目的回顾性分析脑胶质瘤患者术后放射治疗及综合治疗的疗效,寻求胶质瘤治疗的新方法.方法对资料完整的41例胶质瘤患者进行回顾性分析研究,其中低分级胶质瘤23例,高分级胶质瘤14例,少突胶质细胞瘤4例,手术全切29例,次全切12例,20例接受放疗合并颈动脉灌注综合治疗,21例单纯放疗,寿命表法计算生存率并绘制生存曲线.结果综合组及单放组的中位生存期分别为17个月、10个月,kaplan-meier生存曲线分析显示:综合组的生存情况明显高于单放组(1og Rank检验P＜0.05).结论在脑胶质瘤术后放疗过程中同步使用颈动脉灌注榄香烯可改善患者生存时间.     

成人胶质瘤质子与重离子治疗现状及进展

脑胶质瘤是最常见的原发脑恶性肿瘤,标准治疗是手术联合术后放疗,但疗效并不理想。质子和碳离子治疗是目前最先进的放疗技术,在多种肿瘤中显示出优于光子放疗疗效和生存质量。然而,质子与碳离子治疗应用于胶质瘤的作用尚未明确,本文将就质子与碳离子治疗成人胶质瘤的基础研究和临床结果进行详细阐述。     

颅脑

直接皮质刺激运动诱发电位在累及运动区胶质瘤切除术中运动通路保护研究；肺癌脑转移的三维适形放疗；脑恶性胶质瘤术后放化疗联合治疗临床疗效观察；显微手术治疗侧脑室脑瘤（附13例报告）；放疗同步口服替奠唑胺治疗颅内转移瘤疗效评价。[编者按]     

^32P,147Pm对人脑胶质瘤细胞作用

颅内肿瘤在我国居民发病率为1.34/10万,脑胶质瘤约占颅内肿瘤的43％。恶性胶质瘤自然病程从出现症状至死亡平均存活期不到一年。恶性胶质瘤患者术后放疗生存期高于单纯手术治疗。对脑干、丘脑、第三脑室等手术难以达到部位的肿瘤,放疗更具有独特的效果。近年来有人报导采用~(32)P、~(198)Au颅内注射治疗脑胶质瘤。内照射治疗的效果主要取决于选择的核素种类和剂量。为此我们采     

Silencing of R-Spondin1 increases radiosensitivity of glioma cells

Although radiation therapy is the most effective postoperative adjuvant treatment, it does not substantially improve the long-term outcomes of glioma patients because of the characteristic radioresistance of glioma. We found that R-Spondin1 (Rspo1) expression was elevated in high-grade gliomas and was associated with worse overall survival and disease-free survival. Rspo1 expression was also associated with reduced survival rates in glioma patients after treatment with radiotherapy and temozolomide (RT-TMZ). Importantly, Rspo1 was dramatically upregulated after radiation treatment in patients with glioma. Rspo1 silencing by shRNA potentiated glioma cell death upon radiation treatment. In a xenograft nude mouse model, combining radiation and silencing of Rspo1 potentiated tumor growth inhibition. Thus, combining radiotherapy with silencing of Rspo1 is a potential therapeutic approach.     

胶质瘤放疗中国专家共识(2017)中华医学会放射肿瘤治疗学分会

胶质瘤是指起源于神经胶质细胞的肿瘤,是最常见的原发性颅内肿瘤,WHO中枢神经系统肿瘤分类将胶质瘤分为WHO Ⅰ—Ⅳ级,WHOⅠ、Ⅱ级为低级别胶质瘤,Ⅲ、Ⅳ级为高级别胶质瘤。随着现代放疗技术的发展和放射生物学的深入研究,放射治疗已成为胶质瘤的重要治疗手段之一,不同级别胶质瘤的特点不同,放射治疗原则也不尽相同。2016年,我国发布了《中国中枢神经系统胶质瘤诊断与治疗指南》,阐述了胶质瘤的诊断和综合治疗策略,但目前国内尚无针对胶质瘤放疗的相关共识。因此,中华医学会放射肿瘤学分会胶质瘤共识撰写小组对胶质瘤放射治疗中的相关问题达成共识。该共识主要包括WHO Ⅲ、Ⅳ级胶质瘤、WHOⅡ级胶质瘤、弥漫性中线胶质瘤、室管膜瘤、恶性胶质瘤假性进展、胶质瘤脑脊液播散、老年和儿童胶质瘤患者等放疗相关问题。它将围绕临床工作中的焦点问题作出深入分析和归纳总结,力求进一步规范放射治疗技术在胶质瘤治疗中的应用,为大家的临床工作提供循证医学证据和实践指导。     

胶质瘤干细胞对放射线一定抗拒吗?

放射治疗是恶性胶质瘤最重要的辅助治疗方法之一。近年来多数研究表明胶质瘤干细胞相对于非干细胞对于放射线更加抗拒。但是最近有研究表明,胶质瘤干细胞并不一定比传统胶质瘤细胞系抗拒。并且,报道发现微环境有助于胶质瘤细胞放射损伤的修复。以后的研究需要更加重视胶质瘤细胞在体内对于放射线的反应。     

Optimization of combination therapy of arsenic trioxide and fractionated radiotherapy for malignant glioma

PURPOSE: The primary objective was to optimize the combined treatment regimen using arsenic trioxide (ATO) and fractionated radiotherapy for the treatment of malignant glioma. METHODS AND MATERIALS: Nude mice with human glioma xenograft tumors were treated with fractionated local tumor radiation of 250 cGy/fraction/day and 5 mg/kg ATO for 5-10 days. RESULTS: Time course experiments demonstrated that maximal tumor growth delay occurred when ATO was administered between 0 and 4 h after radiation. The combination treatment of ATO and radiation synergistically inhibited tumor growth and produced a tumor growth delay time of 13.2 days, compared with 1.4 days and 6.5 days for ATO and radiation alone (p < 0.01), respectively. The use of concurrent therapy of radiation and ATO initially, followed by ATO as maintenance therapy, was superior to the use of preloading with ATO before combined therapy and produced a tumor growth delay time of 22.7 days as compared with 11.7 days for the ATO preloading regimen (p < 0.01). The maintenance dose of ATO after concurrent therapy was effective and important for continued inhibition of tumor growth. CONCLUSIONS: The combined use of fractionated radiation and ATO is effective for the treatment of glioma xenograft tumors. ATO was most effective when administered 0-4 h after radiation without pretreatment with ATO. These results have important implications for the optimization of treatment regimen using ATO and fractionated radiotherapy for the treatment of brain tumors.     

恶性胶质瘤外照射加X-刀推量的治疗模式的探讨

背景与目的:恶性胶质瘤是预后极差的常见颅内恶性肿瘤,治愈很困难。本研究报告恶性胶质瘤外照射加X刀推量的治疗模式的疗效。方法:对15例确诊为恶性胶质瘤的患者进行了外照射加X-刀推量的治疗。外照射50Gy/25F/5W后,紧接着用X-刀推量7～10Gy。结果:治疗后近期效果满意,无严重神经功能障碍并发症。3例患者分别死于X刀后4、5、11个月,余均健在。全组仅1例在疗后3个月出现脑水肿,给以对症治疗后缓解。余患者无严重的放射反应。结论:恶性胶质瘤外照射加X-刀推量的治疗模式是可行的。     

DNA damage response and repair: insights into strategies for radiation sensitization of gliomas

The incorporation of radiotherapy into multimodality treatment plans has led to significant improvements in glioma patient survival. However, local recurrence from glioma resistance to ionizing radiation remains a therapeutic challenge. The tumoricidal effect of radiation therapy is largely attributed to the induction of dsDNA breaks (DSBs). In the past decade, there have been tremendous strides in understanding the molecular mechanisms underlying DSB repair. The identification of gene products required for DSB repair has provided novel therapeutic targets. Recent studies revealed that many US FDA-approved cancer agents inhibit DSB repair by interacting with repair proteins. This article will aim to provide discussion of DSB repair mechanisms to provide molecular targets for radiation sensitization of gliomas and a discussion of FDA-approved cancer therapies that modulate DSB repair to highlight opportunities for combination therapy with radiotherapy for glioma therapy.     

Re-irradiation for Paediatric Tumours

Despite best available therapy, many children with cancer develop recurrence after multimodal treatment, including initial radiation therapy. Re-irradiation is defined as the use of a second course of radiation therapy with a retreatment volume that overlaps substantially with that of a previously delivered course of radiation therapy. Re-irradiation is an important part of salvage treatment for patients with recurrent ependymoma, diffuse intrinsic pontine glioma, medulloblastoma and germinoma. In patients with ependymoma, conventionally fractionated re-irradiation (1.8 Gy/day) can provide long-term disease control with low rates of high-grade toxicity. For children with progressive diffuse intrinsic pontine glioma, re-irradiation provides effective palliation of symptoms and a survival gain as compared with those treated without re-irradiation. Repeat radiation therapy that includes craniospinal irradiation, if safe to deliver, may provide long-term tumour control in patients with medulloblastoma. Patients with recurrent intracranial germinoma can be effectively salvaged with re-irradiation that includes craniospinal irradiation. Finally, the emerging role of re-irradiation in non-brainstem high-grade glioma and extracranial solid tumours requires further study regarding its efficacy and safety. When given, re-irradiation should be delivered with care so that doses to organs at risk are minimised. In all cases, re-irradiation should be considered as an option alongside, or concurrently with, other salvage treatments, including surgery or systemic therapy, to maximise the likelihood of durable disease control.     

Intractable vomiting from glioblastoma metastatic to the fourth ventricle: three case studies

Dissemination of malignant glioma to the fourth ventricle with metastatic deposits and intractable vomiting is rare. Leptomeningeal extension of malignant glioma is an uncommon condition that has been reported in patients with end-stage disease and is usually unresponsive to any treatment modality. We describe 3 patients with progressing recurrent glioblastoma multiforme in whom leptomeningeal invasion manifested itself as intractable vomiting due to tumor metastases in the floor of the fourth ventricle. All patients received additional radiation therapy focused to the posterior fossa, with complete resolution of vomiting occurring within 10 days after irradiation. The remission of symptoms in these patients persisted until their death 3-4 months after the repeat radiation therapy. These reports indicate that additional focused radiation should be considered because of its significant therapeutic effect in alleviating intractable nausea and vomiting in patients with glioma metastasized to the posterior fossa.     

从分子水平认识和治疗胶质瘤

胶质瘤是神经系统最常见的原发性肿瘤，临床预后还不乐观。我们在临床工作中注意到即使是相同病理类型和级别的胶质瘤，治疗效果存在很大差异。治疗上的差异无疑是重要影响因素，但肿瘤内在的生物学特性，特别是分子水平的差异是关键所在。近年来．神经胶质瘤的诊断和治疗已深入到了分子水平。影像学诊断已不单纯解剖定位，还可以提供分子和功能影像参考：胶质瘤的病理诊断也在组织学分型/分级的基础上进行分子病理分类，并以此为个体化治疗提供参考；治疗开始从传统的手术/放疗/化疗深化到了分子靶向治疗。随着对胶质瘤分子病因/病理机制的深入了解，胶质瘤的临床治疗效果将会进一步提高。     

Combined radiation and gene therapy for brain tumors with adenovirus-mediated transfer of cytosine deaminase and uracil phosphoribosyltransferase genes

Radiation therapy is an established modality for the treatment of malignant gliomas. Several reports have shown the advantage of additional radiation in combination with gene therapy. In this study, we investigated the ability of radiation therapy to enhance 5-fluorocytosine (5-FC)/cytosine deaminase (CD) plus uracil phosphoribosyltransferase (UPRT) gene therapy in malignant gliomas. In vitro study suggested evidence of a significant cytotoxic interaction between radiation therapy and 5-FC/CD + UPRT gene therapy for glioma cells. In vivo experiments demonstrated that the combination of gene therapy and radiation possessed superior antitumor effect in comparison to single therapy. However, the adverse effects of radiation therapy in combination with the gene therapy were observed with respect to normal brain. This combination therapy may be feasible for the treatment of gliomas, although the radiation dose and area should be reduced in order to prevent side effects.