结肠息肉样早癌患者早期血清炎症因子变化

To explore the concentrations alloeosis of the inflammatory factor in blood serum of colonic polypoid nonage carcinoma patients

目的探求结肠息肉样早癌的早期相关性炎症因子及抑癌基因指标,以期为临床早期诊断提供指导。方法通过结肠镜检查结肠息肉样变350例患者,电子结肠镜下息肉行粘膜切除(EMR)或剥离(ESD)后病理学检查证实结肠息肉样早癌变病例120例,检测血清促炎因子TNF-a、IL-6、Cox2及抑炎因子IL-10水平,并检测组织抑癌基因APC、PTEN、PHLPP的表达及230例单纯腺息肉患者与200例查结肠镜提示结肠粘膜正常对照组以上指标进行比较分析。结果病理活检证实结肠息肉癌变组与单纯结肠腺息肉组、正常结肠组比较,血清促炎因子IL-6、Cox2表达量增高(P<0.05),抑炎因子IL-10检测量减低(P<0.01),抑癌基因APC、PTEN、PHLPP,表达水平减低(P<0.01),血清TNF-a无统计学意义。结论对血清一些促炎症因子及抑炎症因子检测水平变化,与结肠息肉组织抑癌基因表达基本相一致,能对部分结肠早癌筛查及诊断提供临床指导,促炎症因子及抑炎症因子可能参与结肠息肉向早癌的演进。

Objective To explore the correlative inflammatory factors and anti-oncogene of colonic polyp nonage carcinoma,to expecte early diagnosis in clinic. Methods The number of patients of colonic polypthrough by coloscopy was 350, by ectomizing mucous membrane of colonic polyp with coloscopy（EMR）or decoherencing（ESD）,and mucous membrane was confirmed nonage carcinoma,these patients were 120,and then to detect the concentrations of TNF-a、IL-6、Cox2 and IL-10 in blood serum,and to detect the expressions of APC 、PTEN、PHLPP,thoses anti-oncogenes in the tissues by EMR or ESD.And the same method,to detect the concentrations of the same factors of those patients whose colonic mucous membrane was adenoid tumor;To detect the concentrations of the same factors of control group 200 patients. Then thoses the concentrations wound to be compared and analyzed. Results The concentrations of IL-6、Cox2 in these patients of confirmed nonage carcinoma in blood serum are higher than in those patients whose colonic mucous membrane was adenoid tumor and in the control group patients,IL-10 is antagonism,the concentrations of APC 、PTEN、PHLPP are as the same as IL-10 with tapering（P〈0.01）.The detect the concentrations of TNF-a is no disparity.Conclusion By detecting the concentration of inflammatory factor and depressive factor like IL-6、Cox2 IL-10,to screen colonic polyp nonage carcinoma,just as detecting the concentrations of APC 、PTEN、PHLPP in the tissues,and also be able to explore the mechanism why adenoid tumor will become to nonage carcinoma.