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

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

in: INT J CANCER, Jahrgang 137, Nr. 10, 15.11.2015, S. 2354-63.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kluth, M, Runte, F, Barow, P, Omari, J, Abdelaziz, ZM, Paustian, L, Steurer, S, Christina Tsourlakis, M, Fisch, M, Graefen, M, Tennstedt, P, Huland, H, Michl, U, Minner, S, Sauter, G, Simon, R, Adam, M & Schlomm, T 2015, 'Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer', INT J CANCER, Jg. 137, Nr. 10, S. 2354-63. https://doi.org/10.1002/ijc.29613

APA

Kluth, M., Runte, F., Barow, P., Omari, J., Abdelaziz, Z. M., Paustian, L., Steurer, S., Christina Tsourlakis, M., Fisch, M., Graefen, M., Tennstedt, P., Huland, H., Michl, U., Minner, S., Sauter, G., Simon, R., Adam, M., & Schlomm, T. (2015). Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer. INT J CANCER, 137(10), 2354-63. https://doi.org/10.1002/ijc.29613

Vancouver

Kluth M, Runte F, Barow P, Omari J, Abdelaziz ZM, Paustian L et al. Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer. INT J CANCER. 2015 Nov 15;137(10):2354-63. https://doi.org/10.1002/ijc.29613

Bibtex

@article{6ca61bc6f94346739ec0c426c8c382eb,
title = "Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer",
abstract = "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 in situ 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 (p < 0.0001 each) and positive surgical margin (p = 0.0004). 16q Deletion was more frequent in ERG fusion-positive (27%) as compared to ERG fusion-negative cancers (16%, p < 0.0001), and was linked to other ERG-associated deletions including phosphatase and tensin homolog (PTEN) (p < 0.0001) and 3p13 (p = 0.0303). In univariate analysis, the deletion of 16q was linked to early biochemical recurrence independently from the ERG status (p < 0.0001). Tumors with codeletions of 16q and PTEN had a worse prognosis (p = 0.0199) than those with PTEN or the deletion of 16q alone. Multivariate modeling revealed that the prognostic value of 16q/PTEN deletion patterns was independent from the established prognostic factors. In summary, the results of our study demonstrate that the deletion of 16q and PTEN cooperatively drives prostate cancer progression, and suggests that deletion analysis of 16q and PTEN could be of important clinical value particularly for preoperative risk assessment of the clinically most challenging group of low- and intermediated grade prostate cancers.",
keywords = "Adult, Aged, Chromosomes, Human, Pair 16, Disease Progression, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Neoplasm Grading, PTEN Phosphohydrolase, Prostatic Neoplasms, Sequence Deletion, Tissue Array Analysis",
author = "Martina Kluth and Frederic Runte and Philipp Barow and Jazan Omari and Abdelaziz, {Zaid M} and Lisa Paustian and Stefan Steurer and {Christina Tsourlakis}, Maria and Margit Fisch and Markus Graefen and Pierre Tennstedt and Hartwig Huland and Uwe Michl and Sarah Minner and Guido Sauter and Ronald Simon and Meike Adam and Thorsten Schlomm",
note = "{\textcopyright} 2015 UICC.",
year = "2015",
month = nov,
day = "15",
doi = "10.1002/ijc.29613",
language = "English",
volume = "137",
pages = "2354--63",
journal = "INT J CANCER",
issn = "0020-7136",
publisher = "Wiley-Liss Inc.",
number = "10",

}

RIS

TY - JOUR

T1 - Concurrent deletion of 16q23 and PTEN is an independent prognostic feature in prostate cancer

AU - Kluth, Martina

AU - Runte, Frederic

AU - Barow, Philipp

AU - Omari, Jazan

AU - Abdelaziz, Zaid M

AU - Paustian, Lisa

AU - Steurer, Stefan

AU - Christina Tsourlakis, Maria

AU - Fisch, Margit

AU - Graefen, Markus

AU - Tennstedt, Pierre

AU - Huland, Hartwig

AU - Michl, Uwe

AU - Minner, Sarah

AU - Sauter, Guido

AU - Simon, Ronald

AU - Adam, Meike

AU - Schlomm, Thorsten

N1 - © 2015 UICC.

PY - 2015/11/15

Y1 - 2015/11/15

N2 - 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 in situ 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 (p < 0.0001 each) and positive surgical margin (p = 0.0004). 16q Deletion was more frequent in ERG fusion-positive (27%) as compared to ERG fusion-negative cancers (16%, p < 0.0001), and was linked to other ERG-associated deletions including phosphatase and tensin homolog (PTEN) (p < 0.0001) and 3p13 (p = 0.0303). In univariate analysis, the deletion of 16q was linked to early biochemical recurrence independently from the ERG status (p < 0.0001). Tumors with codeletions of 16q and PTEN had a worse prognosis (p = 0.0199) than those with PTEN or the deletion of 16q alone. Multivariate modeling revealed that the prognostic value of 16q/PTEN deletion patterns was independent from the established prognostic factors. In summary, the results of our study demonstrate that the deletion of 16q and PTEN cooperatively drives prostate cancer progression, and suggests that deletion analysis of 16q and PTEN could be of important clinical value particularly for preoperative risk assessment of the clinically most challenging group of low- and intermediated grade prostate cancers.

AB - 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 in situ 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 (p < 0.0001 each) and positive surgical margin (p = 0.0004). 16q Deletion was more frequent in ERG fusion-positive (27%) as compared to ERG fusion-negative cancers (16%, p < 0.0001), and was linked to other ERG-associated deletions including phosphatase and tensin homolog (PTEN) (p < 0.0001) and 3p13 (p = 0.0303). In univariate analysis, the deletion of 16q was linked to early biochemical recurrence independently from the ERG status (p < 0.0001). Tumors with codeletions of 16q and PTEN had a worse prognosis (p = 0.0199) than those with PTEN or the deletion of 16q alone. Multivariate modeling revealed that the prognostic value of 16q/PTEN deletion patterns was independent from the established prognostic factors. In summary, the results of our study demonstrate that the deletion of 16q and PTEN cooperatively drives prostate cancer progression, and suggests that deletion analysis of 16q and PTEN could be of important clinical value particularly for preoperative risk assessment of the clinically most challenging group of low- and intermediated grade prostate cancers.

KW - Adult

KW - Aged

KW - Chromosomes, Human, Pair 16

KW - Disease Progression

KW - Humans

KW - In Situ Hybridization, Fluorescence

KW - Male

KW - Middle Aged

KW - Neoplasm Grading

KW - PTEN Phosphohydrolase

KW - Prostatic Neoplasms

KW - Sequence Deletion

KW - Tissue Array Analysis

U2 - 10.1002/ijc.29613

DO - 10.1002/ijc.29613

M3 - SCORING: Journal article

C2 - 26009879

VL - 137

SP - 2354

EP - 2363

JO - INT J CANCER

JF - INT J CANCER

SN - 0020-7136

IS - 10

ER -