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目的:观察GFAP、NT-3、Trk及NCAM在腺样囊性癌(ACC)组织中的表达,探讨ACC嗜神经侵袭可能的分子机制,分析4种蛋白表达与临床各因素的关系。方法:采用免疫组化方法检测94例ACC标本中侵袭相关蛋白表达水平,分析4种蛋白在ACC有无嗜神经侵袭组间和临床各因素组间的表达差异。结果:瘤细胞GFAP、NT-3、Trk的过表达和NCAM的低表达在有无嗜神经侵袭和病理分型组间差异均有统计学意义,P均<0.05;NT-3和Trk的过表达在有无复发组间差异均有统计学意义,P均<0.05;NT-3的过表达在有无切缘浸润组间差异有统计学意义,P<0.05。多因素Logistic回归模型分析表明,GFAP、NT-3和Trk的表达与ACC嗜神经侵袭呈正相关,β分别为2.097、1.871和3.194,P均<0.05;GFAP表达与ACC病理分型呈负相关,β=-1.216,P=0.021。ACC组织中神经组织NCAM的表达高于周围侵袭的肿瘤细胞。结论:瘤细胞过表达GFAP、NT-3和Trk可能共同参与了ACC嗜神经侵袭的过程,低表达NACM对ACC的嗜神经侵袭可能起到了一定的促进作用。
OBJECTIVE: To observe the expression of GFAP, NT-3, Trk and NCAM in adenoid cystic carcinoma (ACC) tissues and to explore the possible molecular mechanism of ACC neuroinvasion and to analyze the relationship between the four protein expressions and clinical factors. Methods: The expressions of invasion-related proteins in 94 ACC specimens were detected by immunohistochemistry. The expression differences of 4 proteins in ACC with or without nerve invasion were analyzed. Results: The overexpression of GFAP, NT-3, Trk and the low expression of NCAM in tumor cells were significantly different between the groups with or without neuropathic invasion and pathological classification (all P <0.05). The NT-3 and Trk overexpression There was significant difference between the two groups in the presence or absence of recurrence (P <0.05). There was a significant difference in the expression of NT-3 between the two groups (P <0.05). Multivariate Logistic regression analysis showed that the expression of GFAP, NT-3 and Trk were positively correlated with ACC neuropathic invasion (β = 2.097, 1.871 and 3.194, respectively, P <0.05). GFAP expression was negatively correlated with ACC pathological classification, β = -1.216, P = 0.021. The expression of NCAM in nerve tissue in ACC tissue was higher than that in surrounding tumor cells. CONCLUSION: Over-expression of GFAP, NT-3 and Trk in tumor cells may participate in the process of ACC neuroinvasion. Low expression of NACM may play a role in promoting neurotoxicity of ACC.