Objective To evaluate the curative effect of neoadjuvant chemotherapy via arterial infusion on advanced colorectal carcinoma. Methods One hundred and twenty-eight advanced colorectal carcinoma patients in stage Ⅱ B or Ⅲ were randomly divided into 2 groups. Sixty-eight cases received preoperative arterial infusion chemotherapy( the treatment group),and chemotherapy regimen consist of Oxaliplatin(L-OHP) 130 mg/m2, Hydroxycamptothecin (HCPT) 20 mg/m2 and Dexifluridine (FUDR)600 mg/m2. Femoral arterial infusion chemotherapy administrated 8 ～ 14 days preoperative. Sixty cases received surgery directly(the control group). The adverse reaction and histology effect after arterial infusion chemotherapy were observed, and resection rate,complications,pathology stage,together with long term survival were compared. Results Adverse reaction were mostly grade Ⅰ -Ⅱ gastrointestinal discomfort and bone marrow depression with arterial infusion chemotherapy. Resection rate was 97. 1% (66/68) ,and 64 cases(96. 9%) underwent raclical (R0) resection in the treatment group, which were higher than those in the the control group(73. 3%(44/60) and 79. 5%,respectively) (x2 = 14. 848,8. 906, Ps ＜ 0. 05). Histology effect of the treatment group was 72. 7%, and the pathology stage downstaged compared to preopeartion. Percent of patients in stage Ⅱ in the treatment group was higher than that in the control group( P ＜ 0. 05). The median survival time of test group was 53. 0 months, 1- ,3-,and 5-year survival rates were 95.3%,85.9% and 44.6%, respectively. In the control group, the median survival time was 42.0 months, 1-, 3-, and 5-year survival rates were 92.6%, 75.9% and 22.0%,respectively. There was significant difference in 5-year survival rate(x2 = 6. 385, P ＜ 0. 05). No difference in postoperative complications between two groups(P ＞ 0. 05). Conclusion The neoadjuvant chemotherapy via arterial infusion is of great significance on downstnging the pathology of advanced colorectal carcinoma, raising the excision rate, especially radical resection, and long term survival rate.

Background and purpose: The previous work of this study has showed that the treatment of liver cancer cells with emodin could induce endoplasmic reticulum (ER) stress and apoptosis. Given the cross-talk between ER stress and autophagy, this study aimed to investigate whether blockage of autophagy, a defense mechanism against environmental stress, could improve the killing effect of emodin on liver cancer cells. Methods: The CYTO-ID auto-phagy detection kit and Western blot were used to determine autophagy in liver cancer cells. After combined treatment with chloroquine (CQ) and emodin, cancer cell survival was analyzed by ATPlite assay and clonogenic assay. Apoptosis was detected by both flow cytometry analysis and Western blot. Results: Autophagy could be induced in liver cancer cells after treatment with emodin. Inhibition of autophagy significantly increased growth-inhibitory effect of emodin on both HepG2 and Huh7 cancer cells. The combination treatment with CQ and emodin promoted remarkable apoptosis in liver cancer cells, evidenced by the increase in the percentage of cells in sub-G1 phase and the higher expression lever of cleaved caspase-3. Conclusion: Therapeutically targeting autophagy is capable of enhancing cytotoxicity of emodin in liver cancer cell lines.