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鼻腔鼻窦鳞癌Skp2和E2F1的表达及临床意义   总被引:1,自引:0,他引:1  
目的研究鼻腔鼻窦鳞状细胞癌和慢性鼻窦炎组织中Skp2和E2F1表达及其临床病理意义。方法49例鼻腔鼻窦鳞状细胞癌、28例慢性鼻窦炎组织常规制作石蜡包埋切片,Spk2和E2F1免疫组化染色。结果鼻腔鼻窦鳞状细胞癌Skp2和E2F1表达阳性率及其评分明显高于慢性鼻窦炎组织(P〈0.01);鼻腔鼻窦中分化鳞状细胞癌、肿块最大径≤3cm、无淋巴结转移及未超出鼻腔鼻窦、侵犯周围组织的病例(临床分型T1N0M0)Skp2和E2F1表达阳性率及评分明显低于低分化鳞状细胞癌;肿块最大径〉3cm、有淋巴结转移及已超出鼻腔鼻窦侵犯周围组织的病例(临床分型T3N1M0、T3N2M0),两者差异有统计学意义(P〈0.01);鼻腔鼻窦鳞状细胞癌组织中Skp2和E2F1表达呈正相关(r=0.623,P〈0.01)。结论skp2和E2F1表达可能是反映鼻腔鼻窦鳞状细胞癌发生、进展、生物学行为和预后的重要生物学标记物。  相似文献   

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Conjugated linoleic acid (CLA) is a term used to describe the different conjugated isomers of linoleic acid. CLA has been found to be anticarcinogenic in mammary cancer, but its effects on colon carcinogenesis are still inconclusive. In this study, the isomer-specific effects of the cis-9, trans-11 and trans-10, cis-12 CLA isomers were investigated in the Min mouse model for intestinal carcinogenesis. The Min mice (n = 10/group) were fed either an AIN-93G control diet or a diet containing 1 g/100 g cis-9, trans-11 or trans-10, cis-12 CLA for 8 wk. The number and size of adenomas were measured and the proteins from the small intestinal tissues extracted for immunoblotting analysis. The number of adenomas did not differ, but the size of the adenomas was greater in the distal part of the small intestine in mice fed the trans-10, cis-12 isomer than in controls (1.19 +/- 0.16 vs. 0.94 +/- 0.21 mm, mean +/- SD, P < 0.01). The same isomer caused an increase in lipid peroxidation, measured as urinary 8-iso-prostaglandin (PG)F(2alpha). Nuclear p65 protein of the mucosal tissue was not detectable in the trans-10, cis-12 group, which differed (P < 0.05) from the control group. Cyclin D1, a target for the nuclear factor (NF)-kappaB pathway, was elevated in the trans-10, cis-12 group compared with the control group (P < 0.01), but cyclooxygenase-2 levels were not higher. There was no difference in beta-catenin protein levels between the groups. The results indicate that the trans-10, cis-12 isomer of CLA can act as a cancer promoter in colon carcinogenesis possibly through pathways affecting NF-kappaB and cyclin D1.  相似文献   

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