ABSTRACT
Objective:To analyze the impact of gender on prognosis in patients with primary hepatocellular carcinoma (HCC) after hepatectomy.Methods:The data of 1 796 patients with HCC who underwent liver resection at the Guangxi Medical University Cancer Hospital from January 2010 to December 2016 were retrospectively analyzed. There were 1 548 males and 248 females, the average age were 49.6 years. Patients were followed up for recurrence and survival. After propensity score matching, the postoperative survival rates of male and female patients were compared. Univariate and multivariate Cox regression was used to analyze independent factors affecting prognosis of patients with HCC after hepatectomy. The age and menopause were analyzed by subgroup analyses.Results:The 1-, 3- and 5-years cumulative overall and recurrence-free survival rates of male patients were significantly lower than that of female patients (all P<0.05). Multivariate analysis showed that female was an independent protective factor affecting postoperative recurrence ( HR=0.777, 95% CI: 0.615-0.982) and overall survival ( HR=0.669, 95% CI: 0.520-0.856). Using a cut-off value of 50 years old, the patients were divided into <50 years old ( n=915) and ≥50 years old ( n=881). In patients who were less than 50 years old, the 1-, 3- and 5-years cumulative overall and recurrence-free survival rates of male patients were significantly lower than those of female patients (all P<0.05). In patients ≥50 years old, there were no significant difference in the cumulative overall and recurrence-free survival rates between male and female patients (all P>0.05). Female patients were then divided into the postmenopausal group ( n=152) and the premenopausal group ( n=96). There were no significant differences in the cumulative overall and cumulative recurrence-free survival rates between the two groups ( P>0.05). Conclusion:The prognosis of female patients with HCC after hepatectomy was significantly better than that of male patients.
ABSTRACT
Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.