title: Polo-like kinase 1 is overexpressed in prostate cancer and linked to higher tumor grades.
abstract: BACKGROUND
  Polo-like kinase 1 (PLK1) is known to be one of the key players in the regulation of mitosis of both normal and malignant transformed cells. Moreover, several studies reported an overexpression of PLK1 in human malignancies compared to the corresponding tissue of origin.
  
  
  METHODS
  In this study, expression of PLK1 was investigated by immunohistochemistry in 78 tissue specimens of prostate carcinoma and in adjacent normal prostate tissue as well as in benign prostate hyperplasia. PLK1 expression was semiquantitavely scored and subsequently correlated to clinicopathological parameters and patient prognosis.
  
  
  RESULTS
  No significant PLK1 expression was observed in normal prostate glandular epithelium and stroma. Specimens of benign prostate hyperplasia were PLK1-negative as well. In contrast, 52.6% of all prostate carcinomas showed strong expression of PLK1. High grade intraepithelial lesions, if present, stained almost invariably in the same manner as the respective invasive tumors. Expression of PLK1 correlated positively with Gleason grade (P = 0.011). No other significant correlations of PLK1 expression with either tumor stage, WHO tumor grade, preoperative PSA, age, or resection margins could be established. In an analysis for differences in PSA-relapse-free survival time, PLK1 expression was not a prognostic marker.
  
  
  CONCLUSIONS
  These results demonstrate a high rate of PLK1-positivity in prostate cancer which suggests involvement of PLK1 in tumorigenesis and progression in this tumor entity. Therefore, targeted strategies focussing on PLK1 inhibition might represent a promising new chemotherapeutic approach in prostate cancer.
authors.affiliation: Institute of Pathology, Charité University Hospital, Berlin, Germany. wilko.weichert@charite.de
authors.forename: Wilko
authors.initials: W
authors.lastname: Weichert
authors.forename: Mathias
authors.initials: M
authors.lastname: Schmidt
authors.forename: Volker
authors.initials: V
authors.lastname: Gekeler
authors.forename: Carsten
authors.initials: C
authors.lastname: Denkert
authors.forename: Carsten
authors.initials: C
authors.lastname: Stephan
authors.forename: Klaus
authors.initials: K
authors.lastname: Jung
authors.forename: Stefan
authors.initials: S
authors.lastname: Loening
authors.forename: Manfred
authors.initials: M
authors.lastname: Dietel
authors.forename: Glen
authors.initials: G
authors.lastname: Kristiansen
mesh_terms: D000368:Aged; D002277:Carcinoma / Q000235:genetics* / Q000473:pathology*; D018797:Cell Cycle Proteins; D002471:Cell Transformation, Neoplastic; D018572:Disease-Free Survival; D020869:Gene Expression Profiling; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D011379:Prognosis; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology*; D011494:Protein Kinases / Q000096:biosynthesis*; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D000097869:Polo-Like Kinase 1
chemical_list: D018797:Cell Cycle Proteins; D011494:Protein Kinases; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D000097869:Polo-Like Kinase 1