Evidence map›Paper›PMID 31549213›Full record

ArticleCancer immunology, immunotherapy : CII2019

The BRCA2 mutation status shapes the immune phenotype of prostate cancer.

Maximilian Jenzer, Peter Keß, Cathleen Nientiedt, Volker Endris, Maximilian Kippenberger, Jonas Leichsenring, Fabian Stögbauer, Josh Haimes, Skyler Mishkin, Brian Kudlow and 11 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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  3. Immune Spatial Organization Predicts Distant Metastasis Risk in Aggressive Localized Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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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

21 authors at 3 institutions in 2 countries.

Maximilian JenzerSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany.
Peter KeßSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany.
Cathleen NientiedtSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany.
Volker EndrisInstitute of Pathology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Maximilian KippenbergerSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany.
Jonas LeichsenringInstitute of Pathology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Fabian StögbauerInstitute of Pathology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Josh HaimesArcherDX, 2477 55th Street, Boulder, CO, 80301, USA.
Skyler MishkinArcherDX, 2477 55th Street, Boulder, CO, 80301, USA.
Brian KudlowArcherDX, 2477 55th Street, Boulder, CO, 80301, USA.
Adam KaczorowskiSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany.
Stefanie ZschäbitzSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany.
Anna-Lena VolckmarInstitute of Pathology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Holger SültmannNational Center for Tumor Diseases, German Cancer Research Center, Cancer Genome Research, Im Neuenheimer Feld 460, 69120, Heidelberg, Germany.
Dirk JägerDepartment of Medical Oncology, University of Heidelberg School of Medicine, National Center for Tumor Diseases (NCT), Im Neuenheimer Feld 460, 69120, Heidelberg, Germany.
Anette DuensingCancer Therapeutics Program, UPMC Hillman Cancer Center, Pittsburgh, USA.
Peter SchirmacherInstitute of Pathology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Markus HohenfellnerDepartment of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Carsten GrüllichDepartment of Medical Oncology, University of Heidelberg School of Medicine, National Center for Tumor Diseases (NCT), Im Neuenheimer Feld 460, 69120, Heidelberg, Germany.
Albrecht StenzingerInstitute of Pathology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany. albrecht.stenzinger@med.uni-heidelberg.de.
Stefan DuensingSection of Molecular Urooncology, Department of Urology, University of Heidelberg School of Medicine, Im Neuenheimer Feld 517, 69120, Heidelberg, Germany. stefan.duensing@med.uni-heidelberg.de.ORCID http://orcid.org/0000-0001-7840-138X
Heidelberg University · DEGerman Cancer Research Center · DEUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in DNA damage repair caused by mutations in BRCA1/2, ATM or other genes have been shown to play an important role in the development and progression of prostate cancer. The influence of such mutations on anti-tumor immunity in prostate cancer, however, is largely unknown. To better understand the correlation between BRCA1/2 mutations and the immune phenotype in prostate cancer, we characterized the immune infiltrate of eight BRCA2-mutated tumors in comparison with eight BRCA1/2 wild-type patients by T-cell receptor sequencing and immunohistochemistry for CD45, CD4, CD8, FOXP3, and CD163. In addition, we analyzed seven prostate cancer biopsies that were either BRCA2 or ATM-mutated in comparison with wild-type tumors. Whereas in BRCA1/2 wild-type tumors, immune cells were found predominantly extratumorally, most BRCA2-mutated tumors including one biopsy showed a significantly increased intratumoral immune cell infiltration. The ratio of intratumoral to extratumoral immune cells was considerably higher in BRCA2-mutated tumors for all markers and reached statistical significance for CD4 (p = 0.007), CD8 (p = 0.006), and FOXP3 (p = 0.001). However, the intratumoral CD8 to FOXP3 ratio showed a trend to be lower in BRCA2-mutated tumors suggesting a more suppressed tumor immune microenvironment. Our findings provide a rationale for the future use of immune oncological approaches in BRCA2-mutated prostate cancer and may encourage efforts to target immunosuppressive T-cell populations to prime tumors for immunotherapy.

Indexed as

Genes, BRCA2MutationCD8 AntigensForkhead Transcription FactorsHumansMalePhenotypeProstatic NeoplasmsT-LymphocytesTumor MicroenvironmentCD8 AntigensForkhead Transcription FactorsFOXP3 protein, humanBRCA1/2Homologous recombination deficiencyImmune checkpoint inhibitorsProstate cancerTumor-infiltrating lymphocytesTumor microenvironment

Identifiers

PMID31549213
PMCPMC6805809
OpenAlexW2975372829

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.