We examined P53 mutation and invasion front grading (IFG) in 30 cases of oral squamous cell carcinomas (OSCCs). The association of P53 mutation and IFG scores with clinicopathological parameters was evaluated. P53 mutation existed in exon 5-8 in 15 out of the 30 OSCCs (50%). The incidence of P53 mutation was not associated with age, gender, N value and TNM stage. However, there was a significant correlation between P53 mutation and T value (P=0.046). There were no statistically significant correlations among the clinicopathological parameters and IFG. Interestingly, The IFG score in OSCCs with P53 mutation was significantly higher than that in OSCCs without P53 mutation (P<0.001). These results suggest that the high incidence of P53 mutation is a major mechanism of OSCC carcinogenesis. The presence of P53 mutation indicates the most anaplastic fields in the invasive areas of the tumors, which may predict poor prognosis for the patients.

AIM:To study lipopolysaccharide (LPS)-stimulated secretion of endothelin-1 (ET-1) and adrenomedullin (Adm) from human vascular endothelial cells (HVEC) and its mechanism. METHODS:In cultured HVEC, LPS was used to stimulate ET-1 and Adm secretion from HVEC. The contents of ET-1 and Adm in medium were determined by radioimmunoassay. RESULTS:LPS stimulated secretion of ET-1 and Adm from HVEC in time-dependent and concentration-dependent manner. The ratio of secreted ET-1 to Adm was not changed compared with the control group. The increase of ET-1 could be inhibited by inhibitor of extracellular signal-regulated protein kinases (PD098059) and inhibitor of P38 kinase (SB202190)（P＜0.01）, while the increase of Adm could only be inhibited by SB202190（P＜0.05）, both had no response to inhibitor of protein kinase C (H7), inhibitor of calmodulin (W7), inhibitor of calcineurin (cyclosporin A) and inhibitor of Ca2+ (nicardipine)（P＞0.05）.CONCLUSION:ERKs and P38 signal pathways may play an important role in the secretion of ET-1 from LPS -stimulated HVEC, while only P38 kinase signal pathway is invovled in the secretion of Adm.

We examined P53 mutation and invasion front grading(IFG)in 30 cases of oral squamous cell carcinomas(OSCCs).The association of P53 mutation and IFG scores with clinicopathological parameters was evaluated.P53 mutation existed in exon 5-8 in 15 out of the 30 OSCCs(50%).The incidence of P53 mutation was not associated with age,gender,N value and TNM stage.However,there was a significant correlation between P53 mutation and T value(P=-0.046).There were no statistically significant correlations among the clinicopathological parameters and IFG.Interestingly,The IFG score in OSCCs with P53 mutation was significantly higher than that in OSCCs without P53 mutation(P<0.001).These results suggest that the high incidence of P53 mutation is a major mechanism of OSCC carcinogenesis.The presence of P53 mutation indicates the most anaplastic fields in the invasive areas of the tumors,which may predict poor prognosis for the patients.

AIM: To study lipopolysaccharide (LPS)-stimulated secretion of endothelin-1 (ET-1) and adrenomedullin (Adm) from human vascular endothelial cells (HVEC) and its mechanism. METHODS: In cultured HVEC, LPS was used to stimulate ET-1 and Adm secretion from HVEC. The contents of ET-1 and Adm in medium were determined by radioimmunoassay. RESULTS: LPS stimulated secretion of ET-1 and Adm from HVEC in time-dependent and concentration-dependent manner. The ratio of secreted ET-1 to Adm was not changed compared with the control group. The increase of ET-1 could be inhibited by inhibitor of extracellular signal-regulated protein kinases (PD 098059 ) and inhibitor of P38 kinase (SB 202190 )( P 0.05).CONCLUSION: ERKs and P38 signal pathways may play an important role in the secretion of ET-1 from LPS -stimulated HVEC, while only P38 kinase signal pathway is invovled in the secretion of Adm.

AIM: To investigate the effect of basic fibroblast growth factor (bFGF) on C-type natriuretic peptide (CNP) production, release and mRNA expression. METHODS: Human endothelial cell cultured; CNP was measured by radioimmunoassay method;CNP mRNA expression was determined by RT-PCR technique. RESULTS: bFGF could augment CNP synthesis in human endothelial cells. Compared with control group,25 ng, 50 ng, 100 ng bFGF increased CNP contents in endothelial cells by 88% (P