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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
The Journal of pathology, 2013-09, Vol.231 (1), p.130-141
Krohn, Antje
Seidel, Annemarie
Burkhardt, Lia
Bachmann, Frederic
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
2013
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Krohn, Antje
Seidel, Annemarie
Burkhardt, Lia
Bachmann, Frederic
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
Titel
Recurrent deletion of 3p13 targets multiple tumour suppressor genes and defines a distinct subgroup of aggressive ERG fusion-positive prostate cancers
Ist Teil von
The Journal of pathology, 2013-09, Vol.231 (1), p.130-141
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2013
Quelle
Wiley-Blackwell Journals
Beschreibungen/Notizen
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. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.4223
Titel-ID: cdi_proquest_miscellaneous_1448223245
Format
–
Schlagworte
3p13 deletion
,
Adenocarcinoma - genetics
,
Adenocarcinoma - metabolism
,
Adenocarcinoma - mortality
,
Adenocarcinoma - pathology
,
Cell Line, Tumor
,
Chromosome Deletion
,
Chromosomes, Human, Pair 3 - genetics
,
Data processing
,
ERG
,
Forkhead Transcription Factors - genetics
,
Forkhead Transcription Factors - metabolism
,
FOXP1
,
Gene Expression Profiling
,
Gene Knockdown Techniques
,
Genes, Tumor Suppressor
,
Germany - epidemiology
,
Humans
,
Kaplan-Meier Estimate
,
Male
,
Neoplasm Recurrence, Local
,
Oligonucleotide Array Sequence Analysis
,
Oncogene Proteins, Fusion - metabolism
,
Polymorphism, Single Nucleotide
,
Prostate - metabolism
,
Prostate - pathology
,
prostate cancer
,
Prostatectomy
,
Prostatic Neoplasms - genetics
,
Prostatic Neoplasms - metabolism
,
Prostatic Neoplasms - mortality
,
Prostatic Neoplasms - pathology
,
PTEN
,
Repressor Proteins - genetics
,
Repressor Proteins - metabolism
,
RYBP
,
SHQ1
,
Tissue Array Analysis
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