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本文引用的文献

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Identification of c-FLIP(L) and c-FLIP(S) as critical regulators of death receptor-induced apoptosis in pancreatic cancer cells.鉴定 c-FLIP(L) 和 c-FLIP(S) 作为胰腺癌细胞中死亡受体诱导凋亡的关键调节因子。
Gut. 2011 Feb;60(2):225-37. doi: 10.1136/gut.2009.202325. Epub 2010 Sep 28.
2
Targeting mutated K-ras in pancreatic adenocarcinoma using an adjuvant vaccine.用辅助疫苗靶向胰腺腺癌中的突变型 K-ras。
Am J Clin Oncol. 2011 Jun;34(3):321-5. doi: 10.1097/COC.0b013e3181e84b1f.
3
Cancer statistics, 2010.癌症统计数据,2010 年。
CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300. doi: 10.3322/caac.20073. Epub 2010 Jul 7.
4
Identification and pre-clinical testing of a reversible cathepsin protease inhibitor reveals anti-tumor efficacy in a pancreatic cancer model.鉴定和临床前试验表明,一种可逆的组织蛋白酶蛋白酶抑制剂在胰腺癌模型中具有抗肿瘤疗效。
Biochimie. 2010 Nov;92(11):1618-24. doi: 10.1016/j.biochi.2010.04.023. Epub 2010 May 4.
5
Correlation between different p53 expression patterns and chromosome 17 imbalances in pancreatic ductal adenocarcinoma based on tissue microarray analysis.基于组织芯片分析的胰腺导管腺癌中不同p53表达模式与17号染色体失衡的相关性
J BUON. 2010 Jan-Mar;15(1):94-100.
6
Activation of EGFR by proteasome inhibition requires HB-EGF in pancreatic cancer cells.蛋白酶体抑制通过 HB-EGF 激活胰腺癌细胞中的 EGFR。
Oncogene. 2010 May 27;29(21):3146-52. doi: 10.1038/onc.2010.52. Epub 2010 Mar 8.
7
A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33.一项全基因组关联研究确定了染色体 13q22.1、1q32.1 和 5p15.33 上的胰腺癌易感性位点。
Nat Genet. 2010 Mar;42(3):224-8. doi: 10.1038/ng.522. Epub 2010 Jan 24.
8
IKKepsilon phosphorylation of estrogen receptor alpha Ser-167 and contribution to tamoxifen resistance in breast cancer.IKKepsilon 对雌激素受体 α Ser-167 的磷酸化作用及其在乳腺癌中对他莫昔芬耐药性的贡献。
J Biol Chem. 2010 Feb 5;285(6):3676-3684. doi: 10.1074/jbc.M109.078212. Epub 2009 Nov 23.
9
Promotion of tumor cell migration by extracellular matrix proteins in human pancreatic cancer.细胞外基质蛋白促进人胰腺癌肿瘤细胞迁移。
Pancreas. 2009 Oct;38(7):804-10. doi: 10.1097/MPA.0b013e3181b9dfda.
10
Deregulation of IKBKE is associated with tumor progression, poor prognosis, and cisplatin resistance in ovarian cancer.IKBKE的失调与卵巢癌的肿瘤进展、预后不良和顺铂耐药相关。
Am J Pathol. 2009 Jul;175(1):324-33. doi: 10.2353/ajpath.2009.080767. Epub 2009 Jun 4.

IκB 激酶 ε 在胰腺导管腺癌中的表达。

IκB Kinase ε expression in pancreatic ductal adenocarcinoma.

机构信息

Anatomic Pathology, Moffitt Cancer Center, Tampa, FL 33612, USA.

出版信息

Am J Clin Pathol. 2011 Jul;136(1):60-6. doi: 10.1309/AJCP2JJGYNIUAS2V.

DOI:10.1309/AJCP2JJGYNIUAS2V
PMID:21685032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4644942/
Abstract

IκB kinase (IKKε) is a serine/threonine protein kinase that belongs to the IKK kinase family. Recent studies have shown that IKKε functions as a breast and ovarian cancer oncogene. We demonstrated frequent overexpression of IKKε in pancreatic ductal adenocarcinoma (PDA). We immunohistochemically evaluated 78 PDAs using the avidin-biotin-peroxidase method and the anti-IKKε rabbit polyclonal antibody. Elevated IKKε reactivity (immunohistochemical score, 4-9) was observed in 64% of PDAs (50/78), but in 0.0% of nonneoplastic pancreatic ductal epithelium (0/113; P < .001). Kaplan-Meier analysis of overall survival revealed that patients with high IKKε-immunohistochemical scores (4-9) had significantly shorter survival than did patients with low IKKε immunohistochemical scores (0-3; P = .023; log-rank test) independent of tumor stage or grade. These data indicate that deregulation of IKKε is a common event in PDA and might have an important role in the pathogenesis of this deadly disease. In addition, IKKε could serve as a prognostic marker and potential therapeutic target for PDA intervention.

摘要

IKK 激酶(IKKε)是一种丝氨酸/苏氨酸蛋白激酶,属于 IKK 激酶家族。最近的研究表明,IKKε 作为乳腺癌和卵巢癌的致癌基因发挥作用。我们证明了 IKKε 在胰腺导管腺癌(PDA)中频繁过表达。我们使用亲和素-生物素-过氧化物酶法和抗 IKKε 兔多克隆抗体,对 78 例 PDA 进行了免疫组织化学评估。在 64%的 PDA(50/78)中观察到 IKKε 反应性升高(免疫组织化学评分 4-9),但在 0.0%的非肿瘤性胰腺导管上皮中(0/113;P<0.001)未观察到。总生存的 Kaplan-Meier 分析显示,高 IKKε 免疫组织化学评分(4-9)的患者的生存时间明显短于低 IKKε 免疫组织化学评分(0-3)的患者(P=0.023;log-rank 检验),与肿瘤分期或分级无关。这些数据表明,IKKε 的失调是 PDA 的常见事件,可能在这种致命疾病的发病机制中发挥重要作用。此外,IKKε 可以作为 PDA 干预的预后标志物和潜在的治疗靶点。