| Endometrial carcinoma is a kind of serious disease that endangers thefemale's health and life, the molecular mechanism of cancer is not fullyunderstood. Generally, the genesis and development of the endometrialcarcinoma is a multi-factor and multi-stage biological behavior, it iscorrelated with many carcinogenic genes and tumor suppressors. C-metgene is carcinogenic gene,was discovered in 1984. It participates incommunicating information in cell, contributes to cellular proliferation,differentiation and motility. P53 is an important tumor suppressor.Abnormal structure and overexpression of C-met and mutation of P53 areclosed associated with the genesis and development of many humancarcinomas. Cellular proliferation and metastasis and invasion are majorfatal reasons of mallignant tumors. They relays on new angiogenesis.PCNA is determinate as a biologic symbol to reflect cellular proliferativeactivities. Microvessel density (MVD) is a gold criterion to estimatetumors' angiogensis. Now, the relationship between C-met and p53expression with cellular proliferative activity,angiogenesis in endometrialcarcinoma hasn't been internally reported. Objective: This study is designed to determine the expression ofC-met,p53,PCNA and CD34 in endometrial adenocarcinoma, in order todiscuss the relationship between C-met and p53 with cellular proliferationand angiogenesis. Method: We determined C-met,p53,PCNA and CD34 expression of 63cases endometrial adenocarcinoma by Immunohistochemical staining (SP) . Results: 1. Among 63 cases endometrial adenocarcinoma, the positiveexpression rate of C-met was 52.38% (33/63), the positive expression rateof p53 was 49.21% (31/63). P53 positive expression rate in group of C-metpositive expression was significantly higher than that in group of C-metnegative expression (P<0.01). 2. It was no significantly difference between the two groups (age≥50 andage<50) that C-met and p53 positive expression rate and PCNA index (PI);MVD in the group of age <50 was higher than that of age≥50 (P<0.05). 3. P53 positive expression rate increased with the increase ofhistological grade (P<0.05). The positive rate of C-met and PI in grade â…¢was higher than gradeâ… and gradeâ…¡(P<0.01), C-met positive rate and PIwas no difference between gradeâ… and gradeâ…¡(P>0.05); MVD in gradeâ…¢was higher than gradeâ… (P<0.05), there was no difference between gradeâ… and gradeâ…¡, gradeâ…¡and grade â…¢(P>0.05). 4. PI increased with the increase of clinical stage (P<0.05). C-metpositive rate and MVD in stage Ⅲ~Ⅳ was higher than in stageâ… and stageâ…¡(P<0.05), there was no difference between stageâ… and stageâ…¡(P>0.05);p53 positive rate in stage Ⅲ~Ⅳ and stageâ…¡was higher than in stageâ… (P<0.05), there was no difference between stage Ⅲ~Ⅳand stageâ…¡(P>0.05). 5. PI increased with the aggravation of myoinvasion (P<0.05). C-metpositive rate and MVD in group of myoinvasion≥1/2 was higher thanthose of myoinvasion <1/2 and myoinvasion =0(P<0.05), there was nodifference between group of myoinvasion <1/2 and that of myoinvasion =0(P>0.05); p 53 positive rate in groups of myoinvasion ≥ 1/2 andmyoinvasion <1/2 was higher than that of myoinvasion =0(P<0.05), therewas no difference between group of myoinvasion≥1/2 and that ofmyoinvasion <1/2(P>0.05). 6. The positive expression rate of C-met and p53 and PI and MVD inlymph nodes metastasis group was significantly higher than those of nolymph nodes metastasis group, respectively (P<0.05). 7. PI and MVD in group of C-met positive expression wassignificantly higher than those of C-met negative expression (P<0.01). 8. PI and MVD in group of p53 positive expression was significantlyhigher than those of p53 negative expression (P<0.01). 9. There was positive correlation between PI and MVD in endometrialadenocarcinoma(r=0.669, P<0.01). 10. The survival rate of patients with positive expression of C-met andp53 and PI≥50 and MVD≥60 decreased, respectively (P<0.05). Conclusion: 1. C-met and p53 expressed in endometrial adenocarcinoma. With theincrease of C-met positive... |