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Kluth, Martina; Runte, Frederic; Barow, Philipp; Omari, Jazan; Abdelaziz, Zaid M.; Paustian, Lisa; Steurer, Stefan; Christina Tsourlakis, Maria; Fisch, Margit; Graefen, Markus; Tennstedt, Pierre; Huland, Hartwig; Michl, Uwe; Minner, Sarah; Sauter, Guido; Simon, Ronald; Adam, Meike; Schlomm, Thorsten

Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer

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  • Media type: E-Article
  • Title: Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer
  • Contributor: Kluth, Martina; Runte, Frederic; Barow, Philipp; Omari, Jazan; Abdelaziz, Zaid M.; Paustian, Lisa; Steurer, Stefan; Christina Tsourlakis, Maria; Fisch, Margit; Graefen, Markus; Tennstedt, Pierre; Huland, Hartwig; Michl, Uwe; Minner, Sarah; Sauter, Guido; Simon, Ronald; Adam, Meike; Schlomm, Thorsten
  • imprint: Wiley, 2015
  • Published in: International Journal of Cancer
  • Language: English
  • DOI: 10.1002/ijc.29613
  • ISSN: 0020-7136; 1097-0215
  • Keywords: Cancer Research ; Oncology
  • Origination:
  • Footnote:
  • Description: <jats:p>The deletion of 16q23‐q24 belongs to the most frequent chromosomal changes in prostate cancer, but the clinical consequences of this alteration have not been studied in detail. We performed fluorescence <jats:italic>in situ</jats:italic> hybridization analysis using a 16q23 probe in more than 7,400 prostate cancers with clinical follow‐up data assembled in a tissue microarray format. Chromosome 16q deletion was found in 21% of cancers, and was linked to advanced tumor stage, high Gleason grade, accelerated cell proliferation, the presence of lymph node metastases (<jats:italic>p</jats:italic> &lt; 0.0001 each) and positive surgical margin (<jats:italic>p</jats:italic> = 0.0004). 16q Deletion was more frequent in <jats:italic>ERG</jats:italic> fusion‐positive (27%) as compared to <jats:italic>ERG</jats:italic> fusion‐negative cancers (16%, <jats:italic>p</jats:italic> &lt; 0.0001), and was linked to other <jats:italic>ERG</jats:italic>‐associated deletions including phosphatase and tensin homolog (<jats:italic>PTEN</jats:italic>) (<jats:italic>p</jats:italic> &lt; 0.0001) and 3p13 (<jats:italic>p</jats:italic> = 0.0303). In univariate analysis, the deletion of 16q was linked to early biochemical recurrence independently from the <jats:italic>ERG</jats:italic> status (<jats:italic>p</jats:italic> &lt; 0.0001). Tumors with codeletions of 16q and <jats:italic>PTEN</jats:italic> had a worse prognosis (<jats:italic>p</jats:italic> = 0.0199) than those with <jats:italic>PTEN</jats:italic> or the deletion of 16q alone. Multivariate modeling revealed that the prognostic value of 16q/<jats:italic>PTEN</jats:italic> deletion patterns was independent from the established prognostic factors. In summary, the results of our study demonstrate that the deletion of 16q and <jats:italic>PTEN</jats:italic> cooperatively drives prostate cancer progression, and suggests that deletion analysis of 16q and <jats:italic>PTEN</jats:italic> could be of important clinical value particularly for preoperative risk assessment of the clinically most challenging group of low‐ and intermediated grade prostate cancers.</jats:p>
  • Access State: Open Access