整联蛋白连接激酶在口腔白斑及早期浸润癌中的表达

目的 研究整联蛋白连接激酶(integrin-linked kinase,ILK)在口腔自斑及早期浸润癌中的表达特点及演变规律,以期为口腔癌前病变的诊断、治疗及口腔癌的预防提供依据.方法 联合应用免疫组织化学及过碘酸希夫反应(periodic acid Schiff reaction,PAS)方法研究ILK在19例正常口腔黏膜(正常黏膜组)、43例白斑伴上皮单纯增生(单纯增生组)、84例白斑伴上皮异常增生异常增生组,包括轻、中度异常增生44例(轻中度异常增生组),重度异常增生和原位癌40例(重度异常增牛组)]及54例早期浸润癌(浸润癌组)中的表达情况及分布规律.结果 ILK在正常口腔黏膜中呈阴性表达,在其他3组中的阳性表达率可高达90%(163/181),并且ILK在间质的表达随病变程度的加重而增加(χ2=41.585,P<0.001).白斑从单纯增生至癌变,ILK的表达呈现从上皮浅层向基底层下移的趋势,基底细胞由阴性转为阳性着色,并且伴随从胞质向胞膜的分布改变.重度异常增生组基底层和间质表达之间差异有统计学意义(P=0.029).ILK在早期浸润癌的癌巢表达较癌旁上皮浅,间质阳性的病例76%(41/54)]较重度异常增生45%(18/40)]增多.结论 ILK在口腔白斑的癌变中可能起莺要作用,确切机制需进一步研究.

Expression of integrin-linked kinase in oral leukoplakia and early invasive carcinoma

Objective To investigate the transmutation and significance of integrin-linked kinase (ILK) in oral leukoplakia and early invasive squamous cell carcinoma.Methods Immunohistochemistry accompanied with periodic acid Schiff reaction (PAS) histochemistry was applied to detect the expression of ILK in 19 normal oral mucosa,43 simple hyperplasia,84 epithelial dysplasia,54 early invasive carcinoma.Results Among the oral leukoplakia and early invasive squamous cell carcinoma.dramatic positive expression of ILK was found in 163/181(90%),but was negative in normal mucosa.ILK staining in stroma exhibited a significantly direct correlation with the exacerbated epithelial dysplasia(χ2=41.585,P<0.001).Along with the oral carcinogenesis,there was an obvious tendency of change-overed ILK staining from superfacial to the basal orientation,the stratum basale diverted into positive,and compared with scattering in cytoplasm.the location of ILK was prone to cytomembrane in epithelium.In severe dysplasia and carcinoma in situ,there was a positive correlation between the basal layer and stroma expression of ILK (P=0.029).It was not only a weaker tincture of ILK in cancer nest than lesional epithelia.but also an augmentation of stroma staining in early invasive squamous cell carcinoma 76%(41/54)]by contrast with severe dysplasia 45%(18/40)].Conclusions The pivotal role of ILK in the regulation of oral carcinogenesis is considerable,however,the precise mechanisms through which ILK affects cellular processes remain to be fully characterized.