Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer. Issue 10 (4th June 2015)

• Record Type: Journal Article
• Authors: 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
• Is Part Of: International journal of cancer. Volume 137:Issue 10(2015:Nov. 15)
• Page Start: 2354
• Page End: 2363
• Publication Date: 2015-06-04
• Subjects: Cancer -- Periodicals; Cancer -- Prevention -- Periodicals; 616.994
• DOI: 10.1002/ijc.29613
• Languages: English
• ISSNs: 0020-7136

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <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 <italic>in situ</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 (<italic>p</italic> < 0.0001 each) and positive surgical margin (<italic>p</italic> = 0.0004). 16q Deletion was more frequent in <italic>ERG</italic> fusion‐positive (27%) as compared to <italic>ERG</italic> fusion‐negative cancers (16%, <italic>p</italic> < 0.0001), and was linked to other <italic>ERG</italic>‐associated deletions including phosphatase and tensin homolog (<italic>PTEN</italic>) (<italic>p</italic> < 0.0001) and 3p13 (<italic>p</italic> = 0.0303). In univariate analysis, the deletion of 16q was linked to early biochemical recurrence independently from the <italic>ERG</italic> status (<italic>p</italic> < 0.0001). Tumors with codeletions of 16q and <italic>PTEN</italic> had a worse prognosis (<italic>p</italic> = 0.0199) than those with <italic>PTEN</italic> or the deletion of 16q alone. Multivariate modeling revealed that the prognostic value of 16q/<italic>PTEN</italic> deletion patterns was independent from the established prognostic factors. In summary, the results of our study demonstrate that the deletion of 16q and <italic>PTEN</italic> cooperatively drives prostate cancer progression, and suggests that deletion analysis of 16q and <italic>PTEN</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.</p> </abstract>