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J Clin Pathol 2006;59:285-288 doi:10.1136/jcp.2005.027672
  • Original article

Overexpression of Pim-1 during progression of prostatic adenocarcinoma

  1. T L Cibull1,
  2. T D Jones1,
  3. L Li2,
  4. J N Eble1,
  5. L Ann Baldridge1,
  6. S R Malott1,
  7. Y Luo3,
  8. L Cheng4
  1. 1Departments of Pathology and Laboratory Medicine, Medicine, Indiana University School of Medicine, Indianapolis, IN and Abbott Laboratories, Abbott Park, IL, USA
  2. 2Departments of Pathology and Laboratory Medicine, and the Division of Biostatistics, Indiana University School of Medicine, Indianapolis, IN and Abbott Laboratories, Abbott Park, IL, USA
  3. 3Abbott Laboratories, Abbott Park, IL, USA
  4. 4Departments of Pathology and Laboratory Medicine, and Urology, Indiana University School of Medicine, Indianapolis, IN and Abbott Laboratories, Abbott Park, IL, USA
  1. Correspondence to:
 Dr L Cheng
 Department of Pathology and Laboratory Medicine, Indiana University Medical Center, University Hospital 3465, 550 North University Blvd., Indianapolis, IN 46202, USA; lcheng{at}iupui.edu
  • Accepted 13 June 2005

Abstract

Aims: Pim-1 is a serine/threonine kinase that has been shown to play an integral role in the development of a number of human cancers, such as haematolymphoid malignancies. Recently, evidence has shown Pim-1 to be important in prostatic carcinogenesis. In order to further our understanding of its role in prostate cancer, we investigated Pim-1 expression in normal, premalignant, and malignant prostate tissue.

Methods: Using immunohistochemistry, Pim-1 expression was analysed in prostate tissue from 120 radical prostatectomy specimens. In each case, Pim-1 staining was evaluated in benign prostatic epithelium, high grade prostatic intraepithelial neoplasia (PIN), and prostatic adenocarcinoma. The number of positively staining cells was estimated, and the intensity of staining was scored on a scale of 0 to 3+.

Results: Pim-1 immunoreactivity was identified in 120 cases (100%) of adenocarcinoma, 120 cases (100%) of high grade PIN, and 62 cases (52%) of benign glands. The number of cells staining in benign epithelium (mean 34%) was much lower than that in high grade PIN (mean 80%; p<0.0001) or adenocarcinoma (mean, 84%; p<0.0001). There was no significant difference between high grade PIN and adenocarcinoma in the percentage of cells staining positively for Pim-1 (p = 0.34). The staining intensity for Pim-1 was significantly lower in benign prostatic epithelium than in PIN and adenocarcinoma (p<0.001). There was no statistically significant correlation between the level of Pim-1 expression and Gleason score, patient age, tumour stage, lymph node metastasis, perineural invasion, vascular invasion, surgical margin status, extraprostatic extension, or seminal vesicle invasion.

Conclusions: Pim-1 expression is elevated in PIN and prostatic adenocarcinoma compared with benign prostatic epithelium. This finding suggests that upregulation of Pim-1 may play a role in prostatic neoplasia.

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