Institute of Pathology Department of Internal Medicine, Charité Universitätsmedizin, Berlin, Germany.
Endocr Relat Cancer. 2011 Jan 13;18(1):181-92. doi: 10.1677/ERC-10-0126. Print 2011 Feb.
Clinical trials indicate efficacy of drugs inhibiting the mammalian target of rapamycin (mTOR) in the treatment of gastroenteropancreatic neuroendocrine tumours (GEP-NET); however, information on detailed expression and activity patterns of mTOR in these tumours is sparse. We investigated the expression of mTOR and expression as well as phosphorylation of its downstream targets 4EBP1, S6K and eIF4E in a cohort of 99 human GEP-NET by immunohistochemistry. We correlated our findings with clinicopathological variables and patient prognosis. We found that 61, 93, 80, 69, 57 and 79% of GEP-NET were positive for mTOR, 4EBP1, cytoplasmic phospho-4EBP1 (p-4EBP1), nuclear p-4EBP1, phospho-S6K (p-S6K) and phospho-eIF4E (p-eIF4E) respectively. mTOR expression and activity were higher in foregut than in midgut tumours. In foregut tumours, expression of mTOR was higher when distant metastases were present (P=0.035). Strong mTOR activity was associated with higher proliferative capacity. In patients with stage IV midgut tumours, strong p-S6K expression was associated with poor disease-specific survival (P=0.048). In conclusion, mTOR shows considerable variations in expression and activity patterns in GEP-NET in dependence of tumour location and metastatic status. We hypothesise that these differences in mTOR expression and activity might possibly influence response to mTOR inhibitors.
临床研究表明,哺乳动物雷帕霉素靶蛋白(mTOR)抑制剂在治疗胃肠胰神经内分泌肿瘤(GEP-NET)方面具有疗效;然而,关于这些肿瘤中 mTOR 的详细表达和活性模式的信息却很少。我们通过免疫组织化学方法研究了 99 个人类 GEP-NET 肿瘤中 mTOR 的表达及其下游靶标 4EBP1、S6K 和 eIF4E 的表达和磷酸化情况。我们将这些发现与临床病理变量和患者预后相关联。我们发现,61%、93%、80%、69%、57%和 79%的 GEP-NET 肿瘤分别对 mTOR、4EBP1、细胞质磷酸化 4EBP1(p-4EBP1)、核磷酸化 4EBP1(p-4EBP1)、磷酸化 S6K(p-S6K)和磷酸化 eIF4E(p-eIF4E)呈阳性。mTOR 的表达和活性在前肠肿瘤中比在中肠肿瘤中更高。在前肠肿瘤中,当存在远处转移时,mTOR 的表达更高(P=0.035)。强烈的 mTOR 活性与更高的增殖能力相关。在患有 IV 期中肠肿瘤的患者中,强烈的 p-S6K 表达与较差的疾病特异性生存相关(P=0.048)。总之,mTOR 在 GEP-NET 中的表达和活性模式因肿瘤位置和转移状态的不同而存在很大差异。我们假设,mTOR 表达和活性的这些差异可能会影响对 mTOR 抑制剂的反应。