ABSTRACT
Objective: This study aims to analyze the therapeutic effect and prognostic factors of carcinoma of parotid gland (CPG). Methods: Data on 103 CPG patients were retrospectively analyzed. The patients were divided into the simple surgery group (Group One) and post-operative radio-chemotherapy group (Group Two). Kaplan-Meier survival analysis, Log-rank test, and Cox re-gression analysis were employed to analyze the five-year overall survival. Chi-square test was applied to compare the local control rate and recurrence-free survival. Logistic regression analysis was used to determine the correlation between all factors and the local control rate. Results:For all patients, the five-year local control rate, five-year recurrence-free survival rate, and five-year overall survival rate were 71.49%, 69.61%, and 76.10%respectively. The five-year local control ratio (81.96%vs. 61.90%), five-year recurrence-free surviv-al (78.69%vs. 59.52%), and five-year overall survival (88.12%vs. 68.50%) were significantly improved in Group Two compared with Group One. The logistic regression analysis showed that the therapeutic method, T staging, as well as pN(+) neck and tumor differentia-tion were significantly correlated to the five-year local control rate and five-year recurrence-free survival (P<0.01). Cox regression anal-ysis showed that therapeutic method, T stage, as well as pN(+) neck and tumor differentiation were significantly correlated to the five-year overall survival (P<0.01). Conclusion:Post-operative radio-chemotherapy can improve the local control and overall survival rates. This therapeutic method is applicable to patients with T3-4 tumors, as well as pN(+) neck and middle-low differentiation.
ABSTRACT
Objective To investigate the mechanism of radiosensitizing effects of endostatin on H-520 human lung squamous cancer cells.Methods H-520 cells was treated with endostatin and/or radiation.Colony-forming assays were used to indicate the radiosensitising effects.Cell cycle distribution and expression of phosphor-p38-MAPK were assayed by FCM,and cyclin D1,cdk2,cdk4 and survivin mRNA leveh were assayed by RT-PCR.Phosphor-Akt was evaluated by Western-blotting.Results Combination of endostatin and irradiation inhibited the proliferation of H-520 cells.According to the colony-forming assays,the D0,Dq,D10 and SF2 values of the combination groups were much lower than those of irradiation groups.The sensitization enhancement ratio(SER)was 1.51.G2/M arrest occurred after 4 Gy irradiation.The gene expression of cyclin D1,cdk2,ckd4 and survivin and phosphor-Akt protein were down-regulated after treatment.The expression of phosphor-p38-MAPK protein was also down-regulated after treatment with 200 μg/ml endostar.Conclusions Endostatin inhibits the growth of H-520 cells and radiosensitizes the cells by induction of G0/G1 arrest,cell apoptosis and down-regulation of gene expression of cyelin D1,cdk2,cdk4 and reduces the phosphorylation of Akt and p38-MAPK.
ABSTRACT
Objective To investigate the radiosensitising effect of recombinant human endostatin (endostar) on human lung squamous cancer cell line H-520 in vitro and its mechanism. Methods H-520 cells in exponential growing phase were treated with endostar alone, irradiation alone, or endostar plus irra-diation. Colony-forming assay was used to investigate the cytotoxicity and radiosensitising effects of endostar. Cell survival fractions of all groups were calculated and cell survival curves were fitted by single-hit multi-tar-get model. Cell apoptosis, cell cycle distribution and activated Caspase expression level were investigated by flow cytometry. Results The D0, Dq, D10 and SF2 values of combined treatment group were much lower than those of irradiation alone group. The sensitization enhancement ratio (SER) was 1.50 (ratio of D0 values). Endnstar induced H-520 cell apoptosis in a dose dependant manner. After administration of endostar, H-520 cell proliferation was inhibited, and cell apoptosis rate and apoptotic bodies were increased. After irradiation of 0 Gy, 2 Gy, 4 Gy and 8 Gy, the apoptosis rate of H-520 cells was 4.27% ±0.29%, 14.3% ±1.15%, 28.49% ± 1.58% and 54.79% ± 1.89% in the radiotherapy alone group, and 22.38% ± 1.61%, 35.01% ±1.16%, 46.83%±2.06% and 64.08%±4.28% in the combined treatment group, respective-ly. The difference between the two groups was significant (t = 19.17, 17.79, 25.64 and 3.44,all P < 0.05 ). Flow cytometric analysis showed that cell cycle distribution changed and G0 + G1 phase arrest oc-curred after endostar treatment, while irradiation induced G2 + M arrest. The expression level of activated Caspase in combination group (62.7% ±1.9% ) was higher compared to the control group ( 12.1%± 0. 1% ) , endostar alone group ( 54.6% ±1.0% ) and irradiation alone group ( 34.1%±1.2% ) ( t = 46.69, 6.55 and 22.54 ; all P < 0.05 ). Conclusion Endostar can enhance the radiosensitivity of H-520 ceils by inhibiting cell proliferation, promoting cell apoptosis and facilitating cell cycle redistribution.