Upregulation of centromere protein F is linked to aggressive prostate cancers
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Upregulation of centromere protein F is linked to aggressive prostate cancers. / Göbel, Cosima; Özden, Cansu; Schroeder, Cornelia; Hube-Magg, Claudia; Kluth, Martina; Möller-Koop, Christina; Neubauer, Emily; Hinsch, Andrea; Jacobsen, Frank; Simon, Ronald; Sauter, Guido; Michl, Uwe; Pehrke, Dirk; Huland, Hartwig; Graefen, Markus; Schlomm, Thorsten; Luebke, Andreas M.
in: CANCER MANAG RES, Jahrgang 10, 2018, S. 5491-5504.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Upregulation of centromere protein F is linked to aggressive prostate cancers
AU - Göbel, Cosima
AU - Özden, Cansu
AU - Schroeder, Cornelia
AU - Hube-Magg, Claudia
AU - Kluth, Martina
AU - Möller-Koop, Christina
AU - Neubauer, Emily
AU - Hinsch, Andrea
AU - Jacobsen, Frank
AU - Simon, Ronald
AU - Sauter, Guido
AU - Michl, Uwe
AU - Pehrke, Dirk
AU - Huland, Hartwig
AU - Graefen, Markus
AU - Schlomm, Thorsten
AU - Luebke, Andreas M
PY - 2018
Y1 - 2018
N2 - Background: Centromere protein F (CENPF) is a key component of the kinetochore complex and plays a crucial role in chromosome segregation and cell cycle progression. Recent work suggests that CENPF upregulation is linked to aggressive tumor features in a variety of malignancies including prostate cancer.Materials and methods: Using a highly annotated tissue microarray, we analyzed CENPF protein expression from a cohort of 8,298 prostatectomized patients by immunohistochemistry to study its effect on prostate-specific antigen recurrence-free survival.Results: CENPF overexpression was found in 53% of cancers, and was linked to higher Gleason grade, advanced pathological tumor stage, accelerated cell proliferation, and lymph node metastasis (p<0.0001, each). A comparison with other key molecular features accessible through the microarray revealed strong associations between CENPF overexpression and presence of erythroblast transformation-specific (ETS)-related gene (ERG) fusion as well as phosphatase and tensin homolog deletion (p<0.0001, each). CENPF overexpression was linked to early biochemical recurrence. A subset analysis revealed that this was driven by the ERG-negative subset (p<0.0001). This was independent of established preoperative and postoperative prognostic parameters in multivariate analyses.Conclusion: The results of our study identify CENPF overexpression as an important mechanism and a potential biomarker for prostate cancer aggressiveness.
AB - Background: Centromere protein F (CENPF) is a key component of the kinetochore complex and plays a crucial role in chromosome segregation and cell cycle progression. Recent work suggests that CENPF upregulation is linked to aggressive tumor features in a variety of malignancies including prostate cancer.Materials and methods: Using a highly annotated tissue microarray, we analyzed CENPF protein expression from a cohort of 8,298 prostatectomized patients by immunohistochemistry to study its effect on prostate-specific antigen recurrence-free survival.Results: CENPF overexpression was found in 53% of cancers, and was linked to higher Gleason grade, advanced pathological tumor stage, accelerated cell proliferation, and lymph node metastasis (p<0.0001, each). A comparison with other key molecular features accessible through the microarray revealed strong associations between CENPF overexpression and presence of erythroblast transformation-specific (ETS)-related gene (ERG) fusion as well as phosphatase and tensin homolog deletion (p<0.0001, each). CENPF overexpression was linked to early biochemical recurrence. A subset analysis revealed that this was driven by the ERG-negative subset (p<0.0001). This was independent of established preoperative and postoperative prognostic parameters in multivariate analyses.Conclusion: The results of our study identify CENPF overexpression as an important mechanism and a potential biomarker for prostate cancer aggressiveness.
KW - Journal Article
U2 - 10.2147/CMAR.S165630
DO - 10.2147/CMAR.S165630
M3 - SCORING: Journal article
C2 - 30519097
VL - 10
SP - 5491
EP - 5504
JO - CANCER MANAG RES
JF - CANCER MANAG RES
SN - 1179-1322
ER -