Evidence map›Paper›PMID 39442954›Full record

ArticleThe Prostate2025

Low SMARCD3 expression is associated with poor prognosis in patients with prostate cancer.

Iris E Ertl, Ursula Lemberger, Pawel Rajwa, Patrik Petrov, Stefan T Mayer, Gerald Timelthaler, Bernhard Englinger, Robert Brettner, Nathalie Garstka, Eva Compérat and 2 more

Abstract read
In one paragraph

Article in The Prostate, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
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

12 authors.

Iris E ErtlDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-7564-9694
Ursula LembergerDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Pawel RajwaDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-4073-6584
Patrik PetrovDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Stefan T MayerDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Gerald TimelthalerCenter for Cancer Research, Medical University of Vienna, Vienna, Austria.
Bernhard EnglingerDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Robert BrettnerDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Nathalie GarstkaDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
Eva CompératDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Lukas KennerDepartment for Experimental and Laboratory Animal Pathology, Clinical Institute of Pathology, Vienna, Austria.
Shahrokh F ShariatDepartment of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.

Funding

"Margaretha-Hehberger-Stiftung", embedded in the "Medizinisch-Wissenschaftlicher Fonds des Bürgermeisters der Bundeshauptstadt Wien", Vienna, Austria 17083
6 · The paper itself

Abstract

backgroundsSWI/SNF complexes represent a family of multi-subunit chromatin remodelers that are affected by alterations in >20% of human tumors. While mutations of SWI/SNF genes are relatively uncommon in prostate cancer (PCa), the literature suggests that deregulation of various subunits plays a role in prostate tumorigenesis. To assess SWI/SNF functions in a clinical context, we studied the mutually exclusive, paralogue accessory subunits SMARCD1, SMARCD2, and SMARCD3 that are included in every known complex and are sought to confer specificity.

methodsPerforming immunohistochemistry (IHC), the protein levels of the SMARCD family members were measured using a tissue microarray (TMA) comprising malignant samples and matching healthy tissue of non-metastatic PCa patients (n = 168). Moreover, IHC was performed in castration-resistant tumors (n = 9) and lymph node metastases (n = 22). To assess their potential role as molecular biomarkers, SMARCD1 and SMARCD3 protein levels were correlated with clinical parameters such as T stage, Gleason score, biochemical recurrence, and progression-free survival.

resultsSMARCD1 protein levels in non-metastatic primary tumors, lymph node metastases, and castration-resistant samples were significantly higher than in benign tissues. Likewise, SMARCD3 protein expression was elevated in tumor tissue and especially lymph node metastases compared to benign samples. While SMARCD1 levels in primary tumors did not exhibit significant associations with any of the tested clinical parameters, SMARCD3 exhibited an inverse correlation with pre-operative PSA levels. Moreover, low SMARCD3 expression was associated with progression to metastasis.

conclusionsIn congruence with previous literature, our results implicate that both SMARCD1 and SMARCD3 may exhibit relevant functions in the context of prostate tumorigenesis. Moreover, our approach suggests a potential role of SMARCD3 as a novel prognostic marker in clinically non-metastatic PCa.

Indexed as

Biomarkers, TumorChromosomal Proteins, Non-HistoneProstatic NeoplasmsAgedHumansImmunohistochemistryLymphatic MetastasisMaleMiddle AgedNeoplasm GradingNeoplasm Recurrence, LocalPrognosisProstatic Neoplasms, Castration-ResistantTranscription FactorsBiomarkers, TumorChromosomal Proteins, Non-HistoneSMARCD1 protein, humanTranscription Factorsprognostic markerprostate cancerSMARCD1SMARCD3SWI/SNF complex

Identifiers

PMID39442954
PMCPMC11648064

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 Socratic graph.