ObjectiveTo evaluate the efficacy and clinical safety of sodium glycididazole (CMNa)in thoracic esophageal squamous carcinoma.Methods From June 1,2008 to October 13,2009,66pathologically proved thoracic esophageal squamous carcinoma (stage Ⅱa-Ⅲ,stage Ⅳ with metastases only in supraclavicular lymph nodes,by AJCC 6th ed) were randomized into radiotherapy plus CMNa (A) or radiotherapy plus placebo (B) group.Radiotherapy was given by conventional schedule:1.8-2.0 Gy per fraction,5 times per week to a total dose of 66 Gy/6.6-7.2w.CMNa was given intravenously 800 mg/m2 3 times a week in solution of 100 ml saline within 30 minutes.Radiotherapy was started 30-60 minutes after completion of infusion.Patients of Group B received placebo in saline solution.A total of 66 patients were enrolled ( Group A:32 ; Group B:34 ),and four patients were unanalyzable,remaining 31 patients in each Group.Baseline factors were balanced.ResultsFollow-up rate was 97％.Group A vs.Group B:the overall response rate was 93.5％ vs.67.7％ ( x2 =6.61,P =0.01 ),2-year overall survival was 39.9％ vs.29.9％ ( x2 =0.62,P =0.433 ),2-year cancer specific survival was 43.1％ vs.26.8％ ( x2 =0.30,P =0.878),and 2-year progression-free survival was 30.1％ vs.27.9％ ( x2 =0.02,P =0.586).No severe side effects observed.All patients tolerated CMNa infusion well.Conclusions CMNa is tolerable and effective as a hypoxic radiosensitizer,and its combination with radiotherapy can improve short term effect.However,survival is not improved within our follow-up period.

The abnormality of serine/threonine kinase Aurora-A is seen in many types of cancers. Although in physiological context it has been shown to play a vital role in cellular mitosis, how this oncogene contributes to tumorigenesis remains unclear. Here we demonstrate that Aurora-A overexpression enhances both the expression level and transcriptional activity of c-Myc. The inhibition of c-Myc expression by RNA interference significantly impaired the oncogenic potential of Aurora-A, resulting in attenuated cellular proliferation and transformation rates as well as fewer centrosomal aberrations. Furthermore, downregulation of c-Myc effectively overcame Aurora-A-induced resistance to cisplatin in esophageal cancer cells. Taken together, our results suggest an important role for c-Myc in mediating the oncogenic activity of Aurora-A, which may in turn allow for future targeting of c-Myc as a potential therapeutic strategy for tumors with Aurora-A overexpression.
Cell Line, Transformed ; Cell Proliferation/drug effects ; Cell Transformation, Neoplastic/drug effects/genetics ; Centro ; Chromo ; Cisplatin/pharmacology ; Down-Regulation ; E ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proto-Oncogene Proteins c-myc/genetics/*metabolism ; RNA, Small Interfering/genetics ; Transcriptional Activation ; Transgenes/genetics