乳腺癌术后放疗诱发放射性肺炎的探讨

目的:分析乳腺癌术后放疗诱发放射性肺炎的临床资料,探讨放疗设野的临床意义.方法:1997至1999年122例乳腺癌患者行胸壁切线、锁骨上野照射,部分行内乳野、腋锁野照射.结果:放射性肺炎多发生在行腋锁野照射的患者.结论:放射性肺炎的发生与腋锁野照射和照射的体积有关,放射时应尽量减少肺的照射体积.     

放疗定位模板在恶性淋巴瘤治疗中的应用

恶性淋巴瘤属常见恶性肿瘤之一[1],放射治疗是其有效的治疗手段,早期病例90%可治愈[2].对于放疗体位的控制如何达到精确水平,无可以参考的依据与标准,技术人员只能凭经验来完成日常工作,尤其是恶性淋巴瘤斗篷野这样较大不规则照射野的模拟定位和治疗中的摆位工作比较复杂,在放射治疗过程中摆位偏差是影响精确治疗的关键[3].     

乳腺癌术后放疗诱发放射性肺炎的探讨

目的：分析乳腺癌术后放疗诱发放射性肺炎的临床资料,探讨放疗设野的临床意义。方法：1997年至1999年122例乳腺癌患者行胸壁切线、锁骨上野照射,部分行内乳野、腋锁野照射。结果：放射性肺炎多发生在行腋锁野的患者。结论：放射性肺炎的发生与腋锁野照射和照射的体积有关,放射时应尽量减少肺的照射体积。     

鼻咽癌简易适形放疗技术的临床应用

目的　提高鼻咽癌患者的局部放疗剂量 ,减少正常组织受量。方法　利用头颈部固定器 ,患者在模拟机下定位设野 ,在治疗机下采模 ,根据患者不同情况采用低熔点铅挡野技术 ,制作与靶区治疗区域相一致的简易适形治疗模块 ,从而大大提高了肿瘤组织的照射剂量 ,有效地保护肿瘤周围正常组织和器官。结果　使用这种方法治疗病人近千例 ,完全重合率达 99%以上 ,这种简易适形在治疗时根据患者不同情况将大脑、小脑、脑干、垂体、眼球等重要组织和器官保护起来 ,大大减少了照射体积 ,提高了鼻咽部肿瘤组织的照射剂量。结论　这种方法简单易行 ,适合广大基层放疗单位应用 ,可提高治疗的准确性和摆位的重复性 ,提高病人的生存率和生存质量。     

三维适形放射治疗计划照射野位置的模拟验证

目的:验证三维适形放疗(3dimentional conformal radiotherapy,3DCRT)计划的照射野精度。方法:应用放射治疗模拟定位机对372例三维适形放疗计划的照射野进行治疗过程模拟,观察其与实际预照射目标的吻合性及铅模质量。结果:在治疗模拟中发现三维适形放疗计划照射野和铅模存在一定误差,最大误差2.1cm,最小误差0.3cm,误差率为5.1%(19/372)。结论:应用放射治疗模拟定位机对三维适形放疗计划照射野精度验证,方法简便,及时纠正了各种误差,可推广使用。     

乳腺癌放疗摆位方法的改进

在常规乳腺癌放疗中,由于摆位使用的是棉枕或海绵枕,稳定性差.乳腺癌锁骨上野和内乳野是仰卧位,腋后野是俯卧位,而该野位于胸部与肩部交接处呈斜面（尤其是偏胖和做了根治术的患者）,小的倾斜度变化就可导致射野大的改变而使体位重复性极差,为此加以改进.     

提高放射治疗摆位精度

目的:探讨放射治疗时如何改进定位器械和摆位方式,在不增加摆位程序的条件下提高摆位治疗的精度。方法:对22位胸腹肿瘤患者分别用热塑定位体模和自己研发的定位辅助器械,进行定位和复位。在20次治疗摆位时,两种模型各用10次,对每一位患者采用相同的摆位条件,摆位后用CBCT在相同条件下采集图像信息,通过XVI系统采用骨模式在相同条件下和参考图像进行匹配,记录数据,观察两种摆位方式哪种精度更高。结果:X,Y,Z三个方向的误差使用辅助器械后治疗精度均有很大提高。结论:采用自己研发的辅助器械后,摆位精度更高。     

体部肿瘤调强放疗采用皮肤定位标记法和体膜定位标记法摆位的精度比较研究

目的:评价体部肿瘤三维适形调强放射治疗(IMRT)的皮肤定位标记与体膜定位标记两种摆位方法的精度差别.方法:将100例体部肿瘤调强放疗的患者随机分为皮肤定位标记和体膜定位标记两组,分别在模拟定位机和治疗加速器上按治疗要求进行体膜固定摆位,并拍摄正侧位XR(模拟机)或EPID(加速器)验证照片,各自与相应的治疗计划DRR...     

上段食管癌应用真空体膜定位修正技术

目的提高食管上段癌放射治疗摆位重复性。方法20例食管上段癌患者分别利用真空体膜进行等中心定位摆位和不使用真空体膜进行定位摆位摄片比较，测量摆位结果与定位片的差距。结果与未使用真空体膜相比，使用真空体膜可明显减少摆位误差。结论真空体膜的应用能减少摆位误差，提高肿瘤放射治疗精度。     

上段食管癌应用真空体膜定位修正技术

目的提高食管上段癌放射治疗摆位重复性。方法20例食管上段癌患者分别利用真空体膜进行等中心定位摆位和不使用真空体膜进行定位摆位摄片比较,测量摆位结果与定位片的差距。结果与未使用真空体膜相比,使用真空体膜可明显减少摆位误差。结论真空体膜的应用能减少摆位误差,提高肿瘤放射治疗精度。     

Tumorigenesis in the brain: location, location, location

Emerging evidence from numerous laboratories supports the notion that brain tumors arise from cells with stem cell/neuroglial progenitor cell properties ("cancer stem cells"). Two recent studies suggest that histologically similar tumors from different brain regions are molecularly distinct because they arise from distinct populations of site-restricted progenitor cells. These new findings imply an interaction between the cell of origin, the tumor microenvironment, and specific cancer-causing genetic changes in the evolution of central nervous system tumors.     

YAP在骨肉瘤细胞中的表达及定位

目的:研究YAP在骨肉瘤细胞中的表达情况和定位。方法:使用SOSP9607、MG63、U2-OS骨肉瘤细胞系和hFOB1.19成骨细胞系,进行qRT-PCR、Western blot实验和荧光共聚焦显微镜观察YAP的表达情况和所在的具体细胞位置。结果:YAP在骨肉瘤细胞中表达量非常高,高于正常的成骨细胞hFOB1.19。YAP在骨肉瘤细胞系中主要表达于细胞核内,而在成骨细胞系中主要表达于细胞质。结论:YAP在骨肉瘤细胞中高表达,在成骨细胞中低表达。在肿瘤细胞中主要位于细胞核内,而在成骨细胞系中主要表达于胞质内。可以推断YAP进入细胞核内,结合下游靶基因,促进肿瘤细胞的生长,参与骨肉瘤细胞的发生。这一发现可以为治疗骨肉瘤提供新的靶点。     

Density-dependent location and interactions of truncated APC and beta-catenin

Adenomatous polyposis coli (APC) is a multifunctional tumour suppressor protein, central to development and the mature organism. It is mutated in most cases of colorectal cancer, rendering it ineffective in mediating beta-catenin degradation. We show that localization of full-length APC in colon carcinoma and noncancer cell lines is independent of cell density. However, the location of truncated APC is a function of cell density and in high-density cells truncated APC is predominantly not nuclear. Although the distribution of truncated APC and beta-catenin is closely linked in subconfluent SW480 cells, at high cell density they are not colocalized. We postulated that in this cell line this could be due to an increase in beta-catenin bound to E-cadherin with formation of adherens junctions at high cell density. However, while in coimmunoprecipitation assays we observe an increase in binding between beta-catenin and E-cadherin and a corresponding decrease in binding between beta-catenin and APC at high cell density, we did not observe a strict colocalization of beta-catenin and E-cadherin at the membrane of all cells.     

Incidence of gliomas by anatomic location

The anatomic location of a glioma influences prognosis and treatment options. The aim of our study was to describe the distribution of gliomas in different anatomic areas of the brain. A representative population-based sample of 331 adults with glioma was used for preliminary analyses. The anatomic locations for 89 patients from a single center were analyzed in more detail from radiologic imaging and recorded on a three-dimensional 1 x 1 x 1-cm grid. The age-standardized incidence rate of gliomas was 4.7 per 100,000 person-years. The most frequent subtypes were glioblastoma (47%) and grade II-III astrocytoma (23%), followed by oligodendroglioma and mixed glioma. The gliomas were located in the frontal lobe in 40% of the cases, temporal in 29%, parietal in 14%, and occipital lobe in 3%, with 14% in the deeper structures. The difference in distribution between lobes remained after adjustment for their tissue volume: the tumor:volume ratio was 4.5 for frontal, 4.8 for temporal, and 2.3 for parietal relative to the occipital lobe. The area with the densest occurrence was the anterior subcortical brain. Statistically significant spatial clustering was found in the three-dimensional analysis. No differences in location were found among glioblastoma, diffuse astrocytoma, and oligodendroglioma. Our results demonstrate considerable heterogeneity in the anatomic distribution of gliomas within the brain.