前列腺癌
前列腺
免疫组织化学
医学
组织微阵列
精囊
单变量分析
人口
病理
内科学
淋巴结
肿瘤科
癌症
多元分析
环境卫生
作者
Shahriar Koochekpour,Siyi Hu,Cruz Vellasco‐Gonzalez,Bernardo Ruiz,Gissu Azabdaftari,Guodong Zhu,Haiyen E. Zhau,Leland W.K. Chung,Robert L. Vessella
出处
期刊:The Prostate
[Wiley]
日期:2011-05-31
卷期号:72 (3): 253-269
被引量:29
摘要
Abstract BACKGROUND We previously cloned prosaposin (PSAP) from metastatic castrate‐resistant prostate cancer (mCRPCa) cells and demonstrated its genomic amplification and/or overexpression in metastatic PCa cell lines, xenografts, and lymph node metastases. The clinicohistopathological significance of serum PSAP levels and its tissue expression and association with predictive or prognostic variable in primary or advanced PCa are not known. METHODS We examined PSAP expression by immunohistochemical staining during early embryogenic development of the prostate and within a large tissue microarray which included 266 benign and malignant prostate tissues. In addition, serum PSAP levels in the age‐adjusted normal male population and in 154 normal individuals and patients with primary or mCRPCa were measured by an ELISA assay. RESULTS Univariate and multivariate analyses revealed a significant and inverse association between PSAP expression and clinical stages II and III tumors, dominant Gleason patterns 3 and 4, and seminal vesicle invasion. In the normal male population, the lowest serum PSAP level was detected before puberty, peaked at the most reproductive age group (20‐ to 39‐year old), and then, decreased to a range between the two groups for men above 40‐year old. Regardless of age and when compared with normal individuals, serum PSAP levels significantly decreased in primary organ‐confined PCa, but increased in those with mCRPCa. CONCLUSION Our results show that PSAP has the potential to differentiate between primary and advanced PCa. Additional large‐scale studies are needed to define the usefulness of tissue expression or serum PSAP levels as a diagnostic or prognostic marker or as a therapeutic target in PCa. Prostate 72:253–269, 2012. © 2011 Wiley Periodicals, Inc.
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