NF—κB和uPA在人脑胶质瘤中的表达

目的 究人脑胶质瘤中核转录因子-κB（NF—κB）和尿激酶型纤溶酶原激活物（uPA）的表达，探讨二者在胶质瘤侵袭性生长和恶性进展中的作用。方法 用免疫组化SP法检测52例脑胶质瘤和5例正常脑组织中NF—κB和uPA的表达和分布情况.结果 NF-κB及uPA在正常脑组织中均未见表达；在52例脑胶质瘤中NF-κB有41例表达，其在高级别胶质瘤中的阳性表达率高于低级别胶质瘤（P〈0．01）。uPA在52例胶质瘤中则全部表达，其在高级别胶质瘤中的表达强度明显高于低级别胶质瘤（P〈0．01）。NF-κB和uPA在胶质瘤中的表达呈正相关（r=0.542，P〈0．01）。结论 脑胶质瘤中，活化的NF-κB可促进uPA表达．从而促进胶质瘤的侵袭性和恶性进展。     

第三脑室后部肿瘤的治疗探讨（附19例临床分析）

目的总结第三脑室后部肿瘤治疗的临床经验。方法回顾性分析2002年1月至2007年12月间收治的19例第三脑室后部肿瘤患者的临床、影像、病理资料及治疗方法。结果19例患者中,手术治疗17例,其中肿瘤全切12例,次全切除5例,术后1例死亡,1例因术后脑积水,行脑室-腹腔分流术;非手术治疗2例,其中单纯内镜造瘘1例,单纯脑室-腹腔分流1例。随访18例,痊愈14例,复发1例,死亡3例。结论第三脑室后部肿瘤大部分可手术切除,结合辅助治疗可治愈或延长患者生命,部分不适于手术切除的患者可姑息治疗,生活质量得到改善。     

Photodynamic Therapy Mediated by 5-Aminolevulinic Acid Suppresses Gliomas Growth by Decreasing the Microvessels

Although 5-aminolevulinic acid(5-ALA)-mediated photodynamic therapy(PDT) has been demonstrated to be a novel and effective therapeutic modality for some human malignancies, its effect and mechanism on glioma are still controversial. Previous studies have reported that 5-ALA-PDT induced necrosis of C6 rat glioma cells in vitro. The aim of this study was to further investigate the effect and mechanism of 5-ALA-PDT on C6 gliomas implanted in rats in vivo. Twenty-four rats bearing similar size of subcutaneously implanted C6 rat glioma were randomly divided into 3 groups: receiving 5-ALA-PDT(group A), laser irradiation(group B), and mock procedures but without any treatment(group C), respectively. The growth, histology, microvessel density(MVD), and apoptosis of the grafts in each group were determined after the treatments. As compared with groups B and C, the volume of tumor grafts was significantly reduced(P<0.05), MVD was significantly decreased(P<0.001), and the cellular necrosis was obviously increased in group A. There was no significant difference in apoptosis among the three groups. The in vivo studies confirmed that 5-ALA-PDT may be an effective treatment for gliomas by inhibiting the tumor growth. The mechanism underlying may involve increasing the cellular necrosis but not inducing the cellular apoptosis, which may result from the destruction of the tumor microvessels.