Abstract

The tumor proliferation index marker Ki-67 is strongly associated with tumor cell proliferation, growth and progression, and is widely used in routine clinicopathological investigation. Prostate cancer is a complex multifaceted and biologically heterogeneous disease, and overtreatment of localized, low volume indolent tumors, is evident. Here, we aimed to assess Ki-67 expression and related outcomes of 535 patients treated with radical prostatectomy. The percentage of tumor epithelial cells expressing Ki-67 was determined by immunohistochemical assay, both digital image analysis and visual scoring by light microscope were used for quantification. The association of Ki-67 and prostate cancer was evaluated, as well as its prognostic value. There was a positive correlation between high expression of Ki-67 and Gleason score > 7 (p < 0.001) as well as tumor size (≥ 20 mm, p = 0.03). In univariate analyses, a high expression of Ki-67 in tumor epithelium was significantly associated with biochemical failure (BF) (digital scoring, p = 0.014) and (visual scoring, p = 0.004). In the multivariate analyses, a high level of Ki-67 was an independent poor prognostic factor for biochemical failure-free survival (BFFS) (Visual scoring, Ki67, p = 0.012, HR:1.50, CI95% 1.10–2.06). In conclusion, high Ki-67 expression is an independent negative prognostic marker for biochemical failure. Our findings support the role of Ki-67 as a significant, poor prognostic factor for in prostate cancer outcome.

Highlights

  • Radical prostatectomy as a primary treatment for clinically localized prostate cancer (PC) has increased dramatically over the past decade due to prostate specific antigen (PSA) screening [1]

  • In this large-scale multi-center study with long-term survival data, we found that a high expression of Ki-67 was an independent predictor for biochemical failure

  • By using visual scorings method, a high Ki-67 was found as an independent predictor for biochemical failure (BF) in multivariate analyses

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Summary

Introduction

Radical prostatectomy as a primary treatment for clinically localized prostate cancer (PC) has increased dramatically over the past decade due to prostate specific antigen (PSA) screening [1]. Despite increased ability to detect cancer, the clinical behavior of PC remains hard to predict as it ranges from indolent to highly aggressive tumors [2]. Management of PC today relies largely on standard clinical. High Ki67 levels predict biochemical failure in prostate cancer

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