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首页> 外文期刊>Diagnostic pathology >Expression of p-AKT characterizes adenoid cystic carcinomas of head and neck with a higher risk for tumor relapses
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Expression of p-AKT characterizes adenoid cystic carcinomas of head and neck with a higher risk for tumor relapses

机译:p-AKT的表达是头颈部腺样囊性癌的特征,具有较高的肿瘤复发风险

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摘要

Background Adenoid cystic carcinomas are rare tumors with an indolent clinical course, but frequent local relapses. The identification of tumors with a higher relapse risk seems to be interesting. Hence we investigated parameters of glucose metabolism, which were found associated with poor prognosis in other malignancies. Methods Specimen of 29 patients were investigated immunohistochemically with antibodies against p-AKT, TKTL-1 (transketolase-like 1), M2PK (M2 pyruvate kinase), and GLUT-1. Proliferation was investigated by staining with Ki67. The tumors were located at the major or minor salivary glands. Only the typical cribriform subtype was investigated. The initial tumor stage was pT1 or pT2. Results Expression of p-AKT was significantly (P = 0.036) associated with a higher relapse risk in multivariate analysis. Low expression of M2PK was non-significantly (P = 0.065) predictive for a higher risk. TKTL-1 and GLUT-1 were expressed in the majority of cases, albeit not associated with relapse risk. Conclusion Adenoid cystic carcinomas positive for p-AKT show a higher relapse risk. However, other parameters of glucose metabolism investigated here or proliferation (Ki67) were not predictive in this entity. Our findings demonstrate a possible background for therapeutic approaches targeting the inhibition of PI3K/AKT pathway.
机译:背景腺样囊性癌是罕见的肿瘤,临床过程缓慢,但局部复发频繁。识别具有较高复发风险的肿瘤似乎很有趣。因此,我们调查了葡萄糖代谢的参数,发现这些参数与其他恶性肿瘤的预后不良有关。方法对29例患者的标本进行了免疫组织化学研究,分别针对p-AKT,TKTL-1(转酮酶样1),M2PK(M2丙酮酸激酶)和GLUT-1的抗体。通过用Ki67染色研究增殖。肿瘤位于主要或次要唾液腺。仅调查典型的筛状亚型。肿瘤的初始阶段是pT1或pT2。结果在多变量分析中,p-AKT的表达显着(P = 0.036)与较高的复发风险相关。 M2PK的低表达无统计学意义(P = 0.065),预示着较高的风险。 TKTL-1和GLUT-1在大多数病例中都有表达,尽管与复发风险无关。结论p-AKT阳性的腺样囊性癌具有更高的复发风险。但是,在此研究的葡萄糖代谢或增殖(Ki67)的其他参数在该实体中不是可预测的。我们的发现证明了靶向抑制PI3K / AKT途径的治疗方法的可能背景。

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