Oral squamous cell carcinoma is a challenging oncology problem.A reliable biomarker for metastasis or high-risk prognosis in oral cancer patients remains undefined.Using quantitative immunohistochemistry,we examined t...Oral squamous cell carcinoma is a challenging oncology problem.A reliable biomarker for metastasis or high-risk prognosis in oral cancer patients remains undefined.Using quantitative immunohistochemistry,we examined the expression of vimentin,E-cadherin,and beta-catenin in 83 oral squamous cell carcinoma patients,and the relationships between the expression of these markers and specific clinicopathological features were analysed.The high expression of vimentin was observed in 23 of 43(53%) tumours from patients who eventually developed a recurrent tumour and was associated with recurrence and death(P < 0.001 and < 0.001,respectively).The decreased expression of E-cadherin was observed in 36 of 43(84%) tumours from patients who eventually developed a recurrent tumour and was also associated with recurrence and death(P < 0.001 and < 0.001,respectively).Although no correlation between beta-catenin expression in whole-tumour sections and clinicopathological features was observed,decreased beta-catenin expression at the tumour invasive front was closely associated with recurrence and death(P=0.002 and 0.002,respectively).The expression of vimentin and that of E-cadherin were associated with survival and were independent prognostic factors in univariate and multivariate analyses.Our data show that the overexpression of vimentin was closely associated with recurrence and death in oral squamous cell carcinoma patients.The combination of the upregulation of vimentin and aberrant expression of E-cadherin/beta-catenin complexes at the tumour invasive front may provide a useful prognostic marker in oral squamous cell carcinoma.展开更多
文摘Oral squamous cell carcinoma is a challenging oncology problem.A reliable biomarker for metastasis or high-risk prognosis in oral cancer patients remains undefined.Using quantitative immunohistochemistry,we examined the expression of vimentin,E-cadherin,and beta-catenin in 83 oral squamous cell carcinoma patients,and the relationships between the expression of these markers and specific clinicopathological features were analysed.The high expression of vimentin was observed in 23 of 43(53%) tumours from patients who eventually developed a recurrent tumour and was associated with recurrence and death(P < 0.001 and < 0.001,respectively).The decreased expression of E-cadherin was observed in 36 of 43(84%) tumours from patients who eventually developed a recurrent tumour and was also associated with recurrence and death(P < 0.001 and < 0.001,respectively).Although no correlation between beta-catenin expression in whole-tumour sections and clinicopathological features was observed,decreased beta-catenin expression at the tumour invasive front was closely associated with recurrence and death(P=0.002 and 0.002,respectively).The expression of vimentin and that of E-cadherin were associated with survival and were independent prognostic factors in univariate and multivariate analyses.Our data show that the overexpression of vimentin was closely associated with recurrence and death in oral squamous cell carcinoma patients.The combination of the upregulation of vimentin and aberrant expression of E-cadherin/beta-catenin complexes at the tumour invasive front may provide a useful prognostic marker in oral squamous cell carcinoma.
文摘目的:通过解吸电喷雾电离质谱成像(desorption electrospray ionization-mass spectrometry imaging,DESI-MSI)研究口腔鳞状细胞癌(oral squamous cell carcinomas,OSCC)的潜在生物标志物和可能的代谢途径。方法:本研究纳入的10例OSCC病例均为在江苏大学附属医院口腔颌面外科就诊住院且接受手术治疗的原发病例。收集组织样本用于DESI-MSI检测,进一步采用多元及单变量统计分析筛选差异代谢物,然后用受试者工作特征曲线(receiver operating characteristic curve,ROC曲线)分析差异代谢物的诊断能力。最后,进行京都基因和基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)代谢通路分析确定相关的代谢通路。结果:OSCC肿瘤组织与正常组织共鉴定出144种差异代谢物,大多数为脂肪酸。ROC曲线分析发现这144种代谢物曲线下的面积(area under the curve,AUC)值均大于0.7。KEGG代谢通路分析发现,与OSCC发生相关的通路为不饱和脂肪酸的生物合成以及脂肪酸的生物合成。结论:基于DESI-MSI筛选了具有诊断价值的差异代谢物,发现OSCC组织存在不饱和脂肪酸的生物合成以及脂肪酸的生物合成代谢紊乱,可能与OSCC的发生发展密切相关。
