[Correlations of p-AKT with PTEN, P53, HER-2 expressions in endometrial carcinoma and their relationship with patient survival].

OBJECTIVE: To investigate the correlation of phosphorylated protein kinase B(p-AKT) with phosphatase and tensin homolog(PTEN), P53,human epidermal growth factor receptor 2(HER-2) expressions in endometrial carcinoma and their significance. METHODS: The expressions of p-AKT with PTEN, HER-2, P53 and Ki67 were assessed in 95 endometrial carcinomas using immunohistochemistry. The biomarker expressions correlated with clinicopathologic variables and with patient survival. RESULTS: (1) p-AKT was positive in 53.7% (51/95) of tumors and was found to express almost similarly in endometrioid adenocarcinoma(EC) and non-enometrioid adenocarcinoma (NEC). There was no significant difference of patient survival between p-AKT positive and negative subgroups (P=0.757). (2) PTEN loss was found in 56.8%(54/95) of tumors, and occurred more often in EC(60.7%, 51/84) than in NEC (27.3%, 3/11), which was of statistical significance (P=0.035). The patients with PTEN loss had a longer survival than those without (P=0.015). (3) Although there was no significant correlation between p-AKT and PTEN expression, the extended analysis showed that the predictive value of PTEN loss in p-AKT positive subgroup (P=0.148) was lower than that in p-AKT negative expression subgroup (P=0.055). Meanwhile p-AKT positive and PTEN loss might have synergic effect on tumor proliferation, Ki67 positive rate was highest in PTEN+/p-AKT+ subgroup (40.0%) and lowest in PTEN-/p-AKT- subgroup (8.7%), which was of significant difference (P=0.015). (4) No correlation was found between p-AKT expression and P53 or HER-2 status (P>0.05). On the other hand, HER-2 and P53 positive correlated significantly (r=0.209, P=0.041) and occurred more frequently in NEC (45.5%, 100.0%) than in EC(6.0%, 42.9%)(P <0.05), which were found to predict poor survival (P<0.05). CONCLUSION: p-AKT was activated equally in EC and NEC. p-AKT positive alone might have limited effect on patient survival, however, p-AKT expression might lower the predictive value of PTEN loss in endometrial carcinoma. Moreover, p-AKT positive and PTEN loss might have synergic effect on tumor proliferation. On the other hand, as p-AKT expression did not have any correlations with PTEN, P53 and HER-2 status in this cohort, there might be other important factors involved in p-AKT activation in endometrial carcinoma. In sum, further investigation should be conducted in the targeted therapy based on p-AKT and associated molecular mechanism in advanced endometrial carcinoma.