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Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers

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Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers. / Krohn, Antje; Seidel, Annemarie; Burkhardt, Lia; Bachmann, Frederik; Mader, Malte; Grupp, Katharina; Eichenauer, Till; Becker, Andreas; Adam, Meike; Graefen, Markus; Huland, Hartwig; Kurtz, Stefan; Steurer, Stefan; Tsourlakis, Maria C; Minner, Sarah; Michl, Uwe; Schlomm, Thorsten; Sauter, Guido; Simon, Ronald; Sirma, Hüseyin.

in: AM J PATHOL, Jahrgang 231, Nr. 1, 01.09.2013, S. 130-41.

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

Harvard

Krohn, A, Seidel, A, Burkhardt, L, Bachmann, F, Mader, M, Grupp, K, Eichenauer, T, Becker, A, Adam, M, Graefen, M, Huland, H, Kurtz, S, Steurer, S, Tsourlakis, MC, Minner, S, Michl, U, Schlomm, T, Sauter, G, Simon, R & Sirma, H 2013, 'Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers', AM J PATHOL, Jg. 231, Nr. 1, S. 130-41. https://doi.org/10.1002/path.4223

APA

Krohn, A., Seidel, A., Burkhardt, L., Bachmann, F., Mader, M., Grupp, K., Eichenauer, T., Becker, A., Adam, M., Graefen, M., Huland, H., Kurtz, S., Steurer, S., Tsourlakis, M. C., Minner, S., Michl, U., Schlomm, T., Sauter, G., Simon, R., & Sirma, H. (2013). Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers. AM J PATHOL, 231(1), 130-41. https://doi.org/10.1002/path.4223

Vancouver

Krohn A, Seidel A, Burkhardt L, Bachmann F, Mader M, Grupp K et al. Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers. AM J PATHOL. 2013 Sep 1;231(1):130-41. https://doi.org/10.1002/path.4223

Bibtex

@article{da8fb5894b1c493fb365b0a6b4048d1a,
title = "Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers",
abstract = "Deletion of 3p13 has been reported from about 20% of prostate cancers. The clinical significance of this alteration and the tumour suppressor gene(s) driving the deletion remain to be identified. We have mapped the 3p13 deletion locus using SNP array analysis and performed fluorescence in situ hybridization (FISH) analysis to search for associations between 3p13 deletion, prostate cancer phenotype and patient prognosis in a tissue microarray containing more than 3200 prostate cancers. SNP array analysis of 72 prostate cancers revealed a small deletion at 3p13 in 14 (19%) of the tumours, including the putative tumour suppressors FOXP1, RYBP and SHQ1. FISH analysis using FOXP1-specific probes revealed deletions in 16.5% and translocations in 1.2% of 1828 interpretable cancers. 3p13 deletions were linked to adverse features of prostate cancer, including advanced stage (p < 0.0001), high Gleason grade (p = 0.0125), and early PSA recurrence (p = 0.0015). In addition, 3p13 deletions were linked to ERG(+) cancers and to PTEN deletions (p < 0.0001 each). A subset analysis of ERG(+) tumours revealed that 3p13 deletions occurred independently from PTEN deletions (p = 0.3126), identifying tumours with 3p13 deletion as a distinct molecular subset of ERG(+) cancers. mRNA expression analysis confirmed that all 3p13 genes were down regulated by the deletion. Ectopic over-expression of FOXP1, RYBP and SHQ1 resulted in decreased colony-formation capabilities, corroborating a tumour suppressor function for all three genes. In summary, our data show that deletion of 3p13 defines a distinct and aggressive molecular subset of ERG(+) prostate cancers, which is possibly driven by inactivation of multiple tumour suppressors.",
keywords = "Adenocarcinoma, Cell Line, Tumor, Chromosome Deletion, Chromosomes, Human, Pair 3, Forkhead Transcription Factors, Gene Expression Profiling, Gene Knockdown Techniques, Genes, Tumor Suppressor, Germany, Humans, Kaplan-Meier Estimate, Male, Neoplasm Recurrence, Local, Oligonucleotide Array Sequence Analysis, Oncogene Proteins, Fusion, Polymorphism, Single Nucleotide, Prostate, Prostatectomy, Prostatic Neoplasms, Repressor Proteins, Tissue Array Analysis",
author = "Antje Krohn and Annemarie Seidel and Lia Burkhardt and Frederik Bachmann and Malte Mader and Katharina Grupp and Till Eichenauer and Andreas Becker and Meike Adam and Markus Graefen and Hartwig Huland and Stefan Kurtz and Stefan Steurer and Tsourlakis, {Maria C} and Sarah Minner and Uwe Michl and Thorsten Schlomm and Guido Sauter and Ronald Simon and H{\"u}seyin Sirma",
note = "Copyright {\textcopyright} 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.",
year = "2013",
month = sep,
day = "1",
doi = "10.1002/path.4223",
language = "English",
volume = "231",
pages = "130--41",
journal = "AM J PATHOL",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers

AU - Krohn, Antje

AU - Seidel, Annemarie

AU - Burkhardt, Lia

AU - Bachmann, Frederik

AU - Mader, Malte

AU - Grupp, Katharina

AU - Eichenauer, Till

AU - Becker, Andreas

AU - Adam, Meike

AU - Graefen, Markus

AU - Huland, Hartwig

AU - Kurtz, Stefan

AU - Steurer, Stefan

AU - Tsourlakis, Maria C

AU - Minner, Sarah

AU - Michl, Uwe

AU - Schlomm, Thorsten

AU - Sauter, Guido

AU - Simon, Ronald

AU - Sirma, Hüseyin

N1 - Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

PY - 2013/9/1

Y1 - 2013/9/1

N2 - Deletion of 3p13 has been reported from about 20% of prostate cancers. The clinical significance of this alteration and the tumour suppressor gene(s) driving the deletion remain to be identified. We have mapped the 3p13 deletion locus using SNP array analysis and performed fluorescence in situ hybridization (FISH) analysis to search for associations between 3p13 deletion, prostate cancer phenotype and patient prognosis in a tissue microarray containing more than 3200 prostate cancers. SNP array analysis of 72 prostate cancers revealed a small deletion at 3p13 in 14 (19%) of the tumours, including the putative tumour suppressors FOXP1, RYBP and SHQ1. FISH analysis using FOXP1-specific probes revealed deletions in 16.5% and translocations in 1.2% of 1828 interpretable cancers. 3p13 deletions were linked to adverse features of prostate cancer, including advanced stage (p < 0.0001), high Gleason grade (p = 0.0125), and early PSA recurrence (p = 0.0015). In addition, 3p13 deletions were linked to ERG(+) cancers and to PTEN deletions (p < 0.0001 each). A subset analysis of ERG(+) tumours revealed that 3p13 deletions occurred independently from PTEN deletions (p = 0.3126), identifying tumours with 3p13 deletion as a distinct molecular subset of ERG(+) cancers. mRNA expression analysis confirmed that all 3p13 genes were down regulated by the deletion. Ectopic over-expression of FOXP1, RYBP and SHQ1 resulted in decreased colony-formation capabilities, corroborating a tumour suppressor function for all three genes. In summary, our data show that deletion of 3p13 defines a distinct and aggressive molecular subset of ERG(+) prostate cancers, which is possibly driven by inactivation of multiple tumour suppressors.

AB - Deletion of 3p13 has been reported from about 20% of prostate cancers. The clinical significance of this alteration and the tumour suppressor gene(s) driving the deletion remain to be identified. We have mapped the 3p13 deletion locus using SNP array analysis and performed fluorescence in situ hybridization (FISH) analysis to search for associations between 3p13 deletion, prostate cancer phenotype and patient prognosis in a tissue microarray containing more than 3200 prostate cancers. SNP array analysis of 72 prostate cancers revealed a small deletion at 3p13 in 14 (19%) of the tumours, including the putative tumour suppressors FOXP1, RYBP and SHQ1. FISH analysis using FOXP1-specific probes revealed deletions in 16.5% and translocations in 1.2% of 1828 interpretable cancers. 3p13 deletions were linked to adverse features of prostate cancer, including advanced stage (p < 0.0001), high Gleason grade (p = 0.0125), and early PSA recurrence (p = 0.0015). In addition, 3p13 deletions were linked to ERG(+) cancers and to PTEN deletions (p < 0.0001 each). A subset analysis of ERG(+) tumours revealed that 3p13 deletions occurred independently from PTEN deletions (p = 0.3126), identifying tumours with 3p13 deletion as a distinct molecular subset of ERG(+) cancers. mRNA expression analysis confirmed that all 3p13 genes were down regulated by the deletion. Ectopic over-expression of FOXP1, RYBP and SHQ1 resulted in decreased colony-formation capabilities, corroborating a tumour suppressor function for all three genes. In summary, our data show that deletion of 3p13 defines a distinct and aggressive molecular subset of ERG(+) prostate cancers, which is possibly driven by inactivation of multiple tumour suppressors.

KW - Adenocarcinoma

KW - Cell Line, Tumor

KW - Chromosome Deletion

KW - Chromosomes, Human, Pair 3

KW - Forkhead Transcription Factors

KW - Gene Expression Profiling

KW - Gene Knockdown Techniques

KW - Genes, Tumor Suppressor

KW - Germany

KW - Humans

KW - Kaplan-Meier Estimate

KW - Male

KW - Neoplasm Recurrence, Local

KW - Oligonucleotide Array Sequence Analysis

KW - Oncogene Proteins, Fusion

KW - Polymorphism, Single Nucleotide

KW - Prostate

KW - Prostatectomy

KW - Prostatic Neoplasms

KW - Repressor Proteins

KW - Tissue Array Analysis

U2 - 10.1002/path.4223

DO - 10.1002/path.4223

M3 - SCORING: Journal article

C2 - 23794398

VL - 231

SP - 130

EP - 141

JO - AM J PATHOL

JF - AM J PATHOL

SN - 0002-9440

IS - 1

ER -