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Hyperactivation of Ha-ras oncogene, but not Ink4a/Arf deficiency, triggers bladder tumorigenesis.Ha-ras癌基因的过度激活而非Ink4a/Arf基因缺失引发膀胱肿瘤发生。
J Clin Invest. 2007 Feb;117(2):314-25. doi: 10.1172/JCI30062. Epub 2007 Jan 25.
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The Akt pathway in human breast cancer: a tissue-array-based analysis.人类乳腺癌中的Akt信号通路:基于组织芯片的分析
Mod Pathol. 2006 Feb;19(2):238-45. doi: 10.1038/modpathol.3800525.
3
Phosphorylated Akt overexpression and loss of PTEN expression in non-small cell lung cancer confers poor prognosis.非小细胞肺癌中磷酸化Akt的过表达和PTEN表达的缺失预示着不良预后。
Lung Cancer. 2006 Feb;51(2):181-91. doi: 10.1016/j.lungcan.2005.10.003.
4
Nuclear-cytoplasmic partitioning of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) differentially regulates the cell cycle and apoptosis.10号染色体缺失的磷酸酶和张力蛋白同源物(PTEN)的核质分配对细胞周期和细胞凋亡有不同的调节作用。
Cancer Res. 2005 Sep 15;65(18):8096-100. doi: 10.1158/0008-5472.CAN-05-1888.
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Expression of activated Akt and PTEN in malignant melanomas: relationship with clinical outcome.活化型Akt和PTEN在恶性黑色素瘤中的表达:与临床结局的关系。
Am J Clin Pathol. 2005 Oct;124(4):528-36. doi: 10.1309/YT58WWMTA6YR1PRV.
6
Differential PTEN protein expression profiles in superficial versus invasive bladder cancers.浅表性与浸润性膀胱癌中PTEN蛋白的差异表达谱
Urol Int. 2005;75(2):102-6. doi: 10.1159/000085933.
7
PI3K/Akt/mTOR pathway as a target for cancer therapy.PI3K/Akt/mTOR信号通路作为癌症治疗的靶点。
Anticancer Drugs. 2005 Sep;16(8):797-803. doi: 10.1097/01.cad.0000173476.67239.3b.
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Potential markers that complement expression of CA125 in epithelial ovarian cancer.可补充CA125在上皮性卵巢癌中表达的潜在标志物。
Gynecol Oncol. 2005 Nov;99(2):267-77. doi: 10.1016/j.ygyno.2005.06.040. Epub 2005 Aug 2.
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Alterations in connexin26 expression during colorectal carcinogenesis.结直肠癌发生过程中连接蛋白26表达的变化
Oncology. 2005;68(2-3):217-22. doi: 10.1159/000086777. Epub 2005 Jul 7.
10
Increased expression of connexin 26 in the invasive component of lung squamous cell carcinoma: significant correlation with poor prognosis.肺鳞状细胞癌侵袭成分中连接蛋白26表达增加:与预后不良显著相关。
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使用组织芯片分析膀胱癌中生物标志物的表达

Analysis of the expression of biomarkers in urinary bladder cancer using a tissue microarray.

作者信息

Harris Loleta D, De La Cerda Jorge, Tuziak Tomasz, Rosen Daniel, Xiao Lianchun, Shen Yu, Sabichi Anita L, Czerniak Bogdan, Grossman H Barton

机构信息

Department of Urology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.

出版信息

Mol Carcinog. 2008 Sep;47(9):678-85. doi: 10.1002/mc.20420.

DOI:10.1002/mc.20420
PMID:18288642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4321940/
Abstract

Dysregulation of Akt, PTEN, Drg-1, Cx-26, and L-plastin expression appear to be important in the progression of various cancers. Their expression in bladder cancer has not been well characterized. To assess the expression of these genes and their relationship to the outcome of bladder cancer, we used a bladder cancer tissue microarray (TMA) of 251 transitional cell carcinomas. We quantitated immunohistochemical staining of each protein using both automated and manual methods and correlated the expression levels with the clinicopathologic characteristics of the tumor and patient survival. Overall, the results from both automated and manual analyses were similar. We found a significant correlation between the expression of PTEN, Cx-26 and L-plastin with known clinically important pathologic features of bladder cancer (tumor grade, stage, and growth pattern). Aberrant localization patterns of Cx-26 and Drg-1 were observed in bladder tumors. There was also a significant correlation in expression among pAkt, PTEN, and L-plastin. Although the expression of these genes correlated with factors known to be associated with patient outcome, none of them was an independent predictor of progression-free or overall survival.

摘要

Akt、PTEN、Drg-1、Cx-26和L-原肌球蛋白表达失调在各种癌症进展中似乎具有重要意义。它们在膀胱癌中的表达尚未得到充分表征。为了评估这些基因的表达及其与膀胱癌预后的关系,我们使用了包含251例移行细胞癌的膀胱癌组织微阵列(TMA)。我们采用自动和手动方法对每种蛋白质的免疫组织化学染色进行定量,并将表达水平与肿瘤的临床病理特征及患者生存率相关联。总体而言,自动分析和手动分析的结果相似。我们发现PTEN、Cx-26和L-原肌球蛋白的表达与已知的膀胱癌重要临床病理特征(肿瘤分级、分期和生长模式)之间存在显著相关性。在膀胱肿瘤中观察到Cx-26和Drg-1的异常定位模式。pAkt、PTEN和L-原肌球蛋白之间的表达也存在显著相关性。尽管这些基因的表达与已知的与患者预后相关的因素相关,但它们均不是无进展生存期或总生存期的独立预测指标。