Radiotherapy is one of major cancer treatment methods.However,radiation resistance is an important reason to restrict the efficacy of radiotherapy and lead to treatment failure.In recent years,the relationship between the canonical Wnt signaling pathway and tumor radiation resistance has more and more attention of the scholars.This review summarized recent ten years findings concerning the canonical Wnt signaling pathway and tumor radiation resistance and tried to find some valuable rules or some internal relationships among different pathways by systemically analyzing.

Objective To investigate the protective effects of (-)-epigallocatechin gallate ( EGCG ) on daunorubicin ( DNR)-induced cardiotoxicity in mice. Methods The qualified mice were randomly divided into four groups:normal control group, myocardial injured model control group,high dose group (80 mg·kg-1 ) and low dose group (40 mg·kg-1 ) of EGCG. EGCG was administered intragastrically once daily for 7 days,followed by a single intraperitoneal injection of DNR (15 mg·kg-1 ) except in the normal control group. The electrocardiogram,myocardial enzymes and TNT-Hs in serum,cardiac ultrastructure of mice were detected after 48 h. Results In DNR model control group,the incidence of arrhythmia was 64. 7%. The activity of serum cardic enzymes including CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs were significantly higher than those in the normal control group(P<0. 01),and myocardial ultrastructure was injured remarkably. The incidence of arrhythmia was 44. 4% in mice treated with high dose of EGCG and 31. 6% in mice with low dose of EGCG. Compared to the model control group, the activity of CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs in serum decreased remarkably in EGCG groups( P<0. 05 or P<0. 01). Low can EGCG alleviated the injury to the ultrastructure of myocardium compared to the model control group. Conclusion EGCG can prevent the cardiac toxicity induced by DNR in mice.

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.

Adjuvant temozolomide-based chemotherapy has become the standard of care for most postoperative glioma patients. However, a large proportion of these patients do not respond to temozolomide. DNA repair enzyme O6-methylguanine-DNA methyl-transferase (MGMT) promoter methylation has emerged as an important molecular marker in patients with gliomas. It is associated with prognosis and resistance to alkylated drugs such as temozolomide. MGMT promoter methylation is the key mechanism of MGMT gene silencing, thereby inhibiting DNA repair and increasing the sensitivity of chemotherapy. We reviewed current data on the prog-nostic and predictive relevance of MGMT testing and clinical trials, summarized the clinical application of MGMT promoter methyla-tion, in order to provide reference for the individualized treatment of glioma patients.

Radiation-induced brain necrosis (RIBN) is a serious late and irreversible complication after radiation therapy for primary or secondary brain tumors as well as head and neck tumors, and there is no effective treatment. In recent years, bevacizumab has been increasingly applied in the treatment of RIBN, which has been proven to yield certain efficacy and improve patient survival. However, the optimal treatment timing and regimen have been controversial and lack of basic consensus. In this article, research progress on these issues was briefly reviewed.

Objective: To detect the expression of NRAGE protein in esophageal squamous cell carcinoma and investigate the relationship between NRAGE and therapeutic effect of radiotherapy. Methods: The expression level of NRAGE in 44 patients with esophageal squamous cell carcinoma was evaluated by immunohistochemistry and statistically analyzed along with clinical data by using multivariate analysis using Cox regression model. Results: The overall expression level of NRAGE protein in esophageal squamous cell carcinoma (P=0.025) and the expression level of NRAGE nuclear protein (P=0.008) were negatively correlated with short-term efficacy. In terms of the overall expression level of NRAGE protein, the 3-year survival rates in the strongly positive group and the positive weakly positive group were 16% and 36%(P=0.198). As for the expression of NRAGE nuclear protein, the 3-year survival rates in the strongly positive group and the positive+ weakly positive group were 0% and 41%(P<0.001). Multivariate analysis using Cox regression model demonstrated that as for the expression of NRAGE nuclear protein, the risk of death in the strongly positive group was significantly higher than those in the positive+ weakly positive group (P=0.002). Conclusion The overall expression level of NRAGE protein in the esophageal cancer is negatively correlated with the short-term efficacy of radiotherapy, whereas it is not correlated with long-term survival rate. The strongly positive expression level of NRAGE nuclear protein is negatively correlated with the short-term efficacy of radiotherapy and the long-term survival rate, prompting that NRAGE may be a molecular indicator for predicting radiation resistance and even the efficacy of radiotherapy for esophageal squamous cell carcinoma