ABSTRACT
Objective:To compare the efficacy and side effects between simultaneous and sequential integrated boost intensity-modulated radiotherapy after operation for high-grade glioma.Methods:We retrospectively analyzed 142 patients with high-grade glioma who underwent postoperative radiotherapy from January 2010 to December 2017. All patients were divided into the simultaneous and sequential integrated boost intensity-modulated radiotherapy groups. Concurrent temozolomide chemotherapy was delivered during radiotherapy in two groups. The follow-up outcomes were statistically compared between two groups.Results:For the whole group, the median overall survival (OS) was 24 months, the median progression-free survival (PFS) was 17 months, and the median disease-free survival (DFS) was 25 months. In the simultaneous and sequential integrated boost intensity-modulated radiotherapy groups, the median OS were 27.2 and 21.0 months ( P=0.950), the median PFS were 21.2 and 15.0 months ( P=0.21), and the median DFS were 28.0 and 18.0 months ( P=0.171), and the disease control rates were 92.86% and 85.17%( P=0.541), respectively. There was no statistical difference in OS, PFS, DFS, short-term efficacy and side effects between two groups. However, the conformity index in the simultaneous integrated boost intensity-modulated radiotherapy group was better than that in the sequential integrated boost intensity-modulated radiotherapy group ( P=0.032). Conclusions:Postoperative simultaneous and sequential integrated boost intensity-modulated radiotherapy yield no statistical differences in the survival, short-term efficacy and side effects in the treatment of high-grade glioma. However, the conformity index in the simultaneous integrated boost intensity-modulated radiotherapy group is significantly better, which can be recommended for postoperative radiotherapy of high-grade glioma.
ABSTRACT
Choroid plexus carcinoma is a relatively rare primary intracranial malignant tumor which is derived from the choroid plexus epithelium.It is classified as World Health Organization (WHO) grade Ⅲ and mainly occurs in children.Currently,maximal surgical resection is still the main therapeutic strategy.The clinical efficacy of postoperative adjuvant therapies remains controversial.Recent studies have promoted that postoperative combination of radiotherapy and chemotherapy can enhance the clinical prognosis and prolong the survival time for choroid plexus carcinoma patients undergoing sub-radical resection.In this review,relevant articles published in the recent 15 years were retrieved to summarize the current status and research progress on the diagnosis and treatment of choroid plexus carcinoma.
ABSTRACT
Objective To investigate the role of NRAGE subcellular localization in the EMT and radioresistance of esophageal cancer cells.Methods EMT model cells were established by the treatment of TE13 cells with TGF-β1.To verify the establishment of EMT model and the phenotype of EMT-like TE13R120 cells,EMT marker mRNA and protein were detected by Real-time PCR and Western blot,respectively.Real-time PCR was also used to detect the expression of NRAGE mRNA in three groups.Total NRAGE protein,cytoplasm protein and nuclear protein were measured by Western blot.Results It was found that TGF-β1 could induce morphological alterations of TE13 cells from epithelial to mesenchymal and change the expressions of EMT maker E-cadherin and vimentin (t =13.56,-232.84,P ＜ 0.05),indicating the successful establishment of EMT model cells.Similar expression trends of EMT makers were observed in TE13R120cells (t=15.84,-54.54,P＜0.05).NRAGE mRNA (t=-8.73,-5.62,P＜ 0.05) and total protein in both EMT model cells and TE13R120 cells were higher than that in TE13 cells,especially for the nuclear proteins.However,no differences in NRAGE cytoplasm protein expression were found among the three groups.In addition,there were also no difference of NRAGE mRNA (t =-0.88,P ＞0.05),cytoplasm and nuclear protein between TE13R120 cells and EMT model cells.Conclusions The radioresistant cell line TE13R120 has the EMT-like phenotype that may cause cell radioresistance by changing the subcelluar localization of NRAGE.