Evidence map›Paper›PMID 32143573›Full record

ArticleMolecular medicine (Cambridge, Mass.)2020

Upregulation of the transcription factor TFAP2D is associated with aggressive tumor phenotype in prostate cancer lacking the TMPRSS2:ERG fusion.

Christoph Fraune, Luisa Harms, Franziska Büscheck, Doris Höflmayer, Maria Christina Tsourlakis, Till S Clauditz, Ronald Simon, Katharina Möller, Andreas M Luebke, Christina Möller-Koop and 16 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

26 authors at 2 institutions in 1 country.

Christoph FrauneInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Luisa HarmsInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Franziska BüscheckInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Doris HöflmayerInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Maria Christina TsourlakisInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Till S ClauditzInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Ronald SimonInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany. R.Simon@uke.de.ORCID 0000-0003-0158-4258
Katharina MöllerInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Andreas M LuebkeInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Christina Möller-KoopInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Stefan SteurerInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Claudia Hube-MaggInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Guido SauterInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Sören WeidemannInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Patrick LebokInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
David DumInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Simon KindInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Sarah MinnerInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Jakob R IzbickiGeneral, Visceral and Thoracic Surgery Department and Clinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Thorsten SchlommDepartment of Urology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Hartwig HulandMartini-Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hans HeinzerMartini-Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Eike BurandtInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Martinistr 52, 20246, Hamburg, Germany.
Alexander HaeseMartini-Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Markus GraefenMartini-Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Cornelia SchroederGeneral, Visceral and Thoracic Surgery Department and Clinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTFAP2D is a transcription factor important for modulating gene expression in embryogenesis. Its expression and prognostic role in prostate cancer has not been evaluated.

methodsTherefore, a tissue microarray containing 17,747 prostate cancer specimens with associated pathological, clinical, and molecular data was analyzed by immunohistochemistry to assess the role of TFAP2D.

resultsTFAP2D expression was typically increased in prostate cancer as compared to adjacent non-neoplastic glands. TFAP2D staining was considered negative in 24.3% and positive in 75.7% of 13,545 interpretable cancers. TFAP2D staining was significantly linked to advanced tumor stage, high classical and quantitative Gleason grade, lymph node metastasis, and a positive surgical margin (p ≤ 0.0045). TFAP2D positivity was more common in ERG fusion positive (88.7%) than in ERG negative cancers (66.8%; p < 0.0001). Subset analyses in 3776 cancers with and 4722 cancers without TMPRSS2:ERG fusion revealed that associations with tumor phenotype and patient outcome were largely driven by the subset of ERG negative tumors. Multivariate analysis did not identify TFAP2D protein expression levels as a robust independent prognostic parameter. Positive TFAP2D immunostaining was significantly associated with 10 of 11 previously analyzed chromosomal deletions in ERG negative cancers (p ≤ 0.0244 each) indicating that elevated TFAP2D expression parallels genomic instability in prostate cancer.

conclusionThese data demonstrate that TFAP2D protein overexpression is linked to prostate cancer progression and genomic instability in ERG negative prostate cancers.

Indexed as

Up-RegulationAdultAgedAged, 80 and overChromosome DeletionGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLymphatic MetastasisMaleMargins of ExcisionMiddle AgedNeoplasm StagingOncogene Proteins, FusionPrognosisProstatic NeoplasmsOncogene Proteins, FusionTFAP2D protein, humanTMPRSS2-ERG fusion protein, humanTranscription Factor AP-2genomic instabilityimmunohistochemistryprognosisprostate cancerTFAP2Dtissue micro array

Identifiers

PMID32143573
PMCPMC7060561
OpenAlexW3011648580

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.