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作 者:郑旭[1] 孙保存[1,2] 赵秀兰[1] 王进京[1] 董学易[1] 古强[1] 孙冉[1]
机构地区:[1]天津医科大学病理教研室,天津市300070 [2]天津医科大学附属肿瘤医院病理科
出 处:《中国肿瘤临床》2013年第8期431-435,共5页Chinese Journal of Clinical Oncology
基 金:国家自然科学基金重点项目(编号:81230050);国家自然科学基金面上项目(编号:81172046;81173091)资助~~
摘 要:目的:研究肺肉瘤样癌(pulmonary sarcomatoid carcinoma,PSC)中血管生成拟态(vasculogenic mimicry,VM)的临床意义,阐述上皮间充质转化(epithelial-to-mesenchymal transition,EMT)提高PSC的恶性度及促进VM形成的相关机制。方法:对肺肉瘤样癌组织切片22例进行HE、CD31和PAS双重染色,Twist、Vimentin、E-cadherin、VEGF免疫组织化学染色,分析VM相关的临床意义及EMT促进VM形成的相关机制。结果:22例中4例(18.2%)存在VM,Kaplan-Meier生存分析提示有无VM肿瘤患者比较生存时间差异有统计学意义(P<0.05)。VM阳性患者Twist的阳性率较阴性患者高,且差异有统计学意义(P<0.05)。Twist1的表达与VEGF、E-cadherin、Vimentin的表达存在明显相关性。结论:VM是患者预后的不利因素,肺肉瘤样癌中发生了EMT,转录因子Twist1可能通过下调E-cadherin,上调Vimentin诱导EMT,并可能通过上调VEGF的表达促进VM的形成,从而促进肿瘤的侵袭和转移。Objective: The expression and clinical significance of vasculogenic mimicry (VM) were investigated. The related mechanisms of epithelial-to-mesenchymal transition (EMT) in VM formation and worsening of puhnonary sarcomatoid carcinoma (PSC) were examined. Methods: Hematoxylin and eosin staining, CD31/periodic acid-Schiff double staining, and immunohistochemi- cal staining were performed to determine the expression of VM, Twist l, vascular endothelial growth factor (VEGF), E-cadherin, and vi- mentin in the tissues of 22 PSC patients. The clinical significance of VM and the mechanism of EMT in VM formation were explored. Results: VM was found in four (18.2%) of the 22 PSC patients. Kaplan Meier survival analysis revealed that the patients with VM had a shorter survival period than those without the VM expression, with statistically significant differences found between the two groups. Comparative results of the groups with and without VM expression showed a higher positive rate of Twistl expression in the former group (P〈0.05). Significant correlations were observed between the Twistl expression and the VEGF, E-cadherin, and vimentin expression. Conclusion: VM unfavorably influences the prognosis of PSC patients. Twistl can upregulate Vimentin and downregulate E-cadherin by inducing EMT. Additionally, it may upregulate VEGF to promote VM formation, which increases tumor invasions and metastases.
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