结直肠癌中pERK1/2和pAKT表达模式的临床病理意义以及预测预后的价值

The pattern of expression of pERK1/2 and pAKT is association with the progression of colorectal cancer but not with the prognosis

目的探讨磷酸化蛋白pERK1/2、pAKT在结直肠癌中表达的意义以及它们用于预测预后的价值。方法运用免疫组化法检测84例结直肠癌手术标本、癌旁正常黏膜pERK1/2、pAKT表达模式,13例腹部创伤手术患者的正常结直肠黏膜做为对照。分析pERK1/2、pAKT表达模式与临床病理特征以及生存预后的关系。结果 pERK1/2、pAKT表达率从癌灶(65.5%、58.3%)到癌旁(45.2%、44.0%)和对照组(30.8%、15.4%)依次降低,P<0.05;它们与肿瘤的大小、浸润深度、分化程度、T和N分期显著正相关;pERK1/2和pAKT双阳性表达病例、单阳病例、双阴病例的5年生存率和中位生存时间在趋势上依次升高,但差异无统计学意义,P>0.05。结论 ERK1/2、pAKT异常激活是结直肠癌的一个特征变化,二者磷酸化表达水平上调与肿瘤进展、侵袭性增强相关,但是目前的数据尚不支持pERK1/2、pAKT可以作为预测预后的独立因子。

Objective To investigate whether the expressions of phosphorylated proteins,pERK1/2 and pAKT are associated with the clinic pathologic features of colorectal cancer （CRC） and prognosis.Methods Immunostainning of pERK1/2 and pAKT was emplored to decete the paraffin slides derived from 84 samples of CRC and normal mucosa adjacent to the cancer,and 13 samples of abdominal injury people＇ normal colorectal mucosa that were considered as control group.Spearman correlation anlysis and life table method were conducted to explore if the two phosphorylated proteins expressions were associated with the clinic pathologic features and prognosis.Results The expressions of pERK1/2 and pAKT decreased gradually in the cohort of from CRC （65.5％,58.3％） to normal mucosa （45.2％,44.0％） and control （30.8％,15.4％） （P ＜0.05）.Moreover,the expression of pERK1/2 and pAKT were significantly correlated with the tumor size,the depth of invasion,the differentiation and T/N stage.Although the cases of pERK1/2 and pAKT double stained displayed lower 5-year survival rate and shorter median survival time in trend by comparison with those cases of single stained or double negative stained,there were no significant differences （P ＞0.05）.Conclusion The aberrant activations of ERK1/2 and AKT were considered as a character of CRC,and the up-regulations of them at phosphorylated levels were involved in the tumor progression and the enhanced invasive potential; however,the current data failed to support the hypothesis that the both of them were treated as independent prognostic factors for CRC.