喉鳞癌组织中SMG-1、ATM和P53的表达及临床意义

Expressions of SMG-1, ATM and P53 in laryngeal squamous cell carcinoma and their clinical significance

目的检测SMG-1、ATM和P53在喉鳞癌组织中的表达,探讨它们在肿瘤发生发展过程中的相互作用。方法收集2006年1月1日~2009年8月31日在耳鼻咽喉科住院手术的喉鳞癌患者标本,采用免疫组化法检测63例喉鳞癌、30例癌旁正常组织中SMG-1、ATM和P53蛋白的表达情况,并对它们的表达与喉癌临床病理特征之间的关系以及三者的相关性进行分析。结果SMG-1、ATM和P53在喉鳞癌组中的表达率分别为36.5%（23/63）、41.3%（26/63）、和57.1%（36/63）,与癌旁正常组织比较（分别为73.3%、83.3%、和20.0%）,差异有统计学意义（P〈0.05）;SMG-1表达与T分期和原发部位呈显著相关（P〈0.05）,与患者年龄、N分期、病理分级无关（P〉0.05）。ATM和P53表达均与患者年龄、T分期、N分期、原发部位、病理分级无关（P〉0.05）。SMG-1阴性表达患者的五年生存率明显高于阳性患者,差异有统计学意义（P〈0.05）。SMG-1和P53的表达之间存在负相关关系（r=-0.476,P〈0.01）。结论 SMG-1、ATM和P53与喉癌的发生关系密切,SMG-1表达是反映喉癌临床病理特征和预后的重要生物学指标,其可能通过调控P53表达,共同在喉癌的发生发展中起重要作用。

Objective To detect the expression of SMG-1, ATM and P53 in laryngeal squamous cell carcinoma（LSCC） and their correlation with the clinicopathological features and outcomes of the patients. Methods Sixty- three specimens of surgically resected LSCC tissues and 30 specimens of adjacent normal tissue were examined for the expressions of ATM, SMG-1 and P53 using immunohistochemistry. The correlation of ATM, SMG- 1 and P53 expressions with the clinicopathological factors and their interactions were analyzed. Results The positive expression rates of SMG-1, ATM and P53 in LSCC were 36.5%（23/63）,41.3%（26/63） and 57.1%（36/63） respectively, significantly different from those in the adjacent tissue（73.3%, 83.3% and 20.0%,respectively; P0.05）. The expression of SMG- 1 in LSCC was positively correlated with the pathological grade and T stage of the tumors（P0.05）, and ATM and P53 were not related to the clinicopathological factors（P0.05）. The 5-year survival rate of patients negative for SMG-1 expression was significantly higher than that of SMG-1-positive patients（P0.05）. The expression of SMG-1 was negatively correlated with that of P53（r=-0.476, P0.01）. Conclusion SMG-1, ATM and P53 are closely related to the occurrence of LSCC. SMG- 1 expression is an important factor associated with the clinicopathological features and prognosis of LSCC patients, and may play an important role in the development of LSCC by regulating P53 expression.