ArticlePloS one2025
Clinical feature and gene expression analysis in low prostate-specific antigen, high-grade prostate cancer.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProstate cancer (PCa) patients with low prostate-specific antigen (PSA) levels can occasionally present high-grade disease. These patients often exhibit resistance to androgen deprivation therapy and have poor outcomes. The mechanisms underlying these observations remain poorly understood. This study aimed to investigate the clinical characteristics and potential gene expression mechanisms in this subgroup. PATIENTS AND
methodsClinical data from 365,558 PCa patients were categorized into four groups based on PSA levels and Gleason score (GS): Group 1 (PSA ≤ 2.5 ng/mL, GS < 8), Group 2 (PSA ≤ 2.5 ng/mL, GS ≥ 8), Group 3 (PSA > 2.5 ng/mL, GS < 8), and Group 4 (PSA > 2.5 ng/mL, GS ≥ 8). Clinical characteristics were compared using Kruskal-Wallis H and Pearson's chi-squared tests. Competing-risks regression assessed prostate cancer-specific mortality (PCSM). Gene set enrichment analysis (GSEA) was performed on 219 PCa patients to compare Group A (PSA ≤ 2.5 ng/mL, GS ≥ 8) with Group B (PSA > 2.5 ng/mL, GS ≥ 8).
resultsGroup 2 had a significantly higher tumor stage (p < 0.001) and increased hazard ratio for PCSM (p < 0.001). GSEA in Group A identified 156 upregulated gene sets and highlighted several enriched pathways, including the polycomb repressive complex 2, the epidermal growth factor receptor family, retrograde axonal transport, the tumor necrosis factor/nuclear factor-κB pathway, the Rho guanine nucleotide exchange factor/RhoA pathway, and the phosphoinositide 3-kinase signaling pathways (p < 0.05, false discovery rate-adjusted p < 0.25).
conclusionPCa patients with low PSA levels and high GS demonstrated an increased risk of PCSM. They were characterized by the aberrant activation of multiple signaling pathways. Targeted therapeutic strategies aimed at these pathways warrant further investigation for their potential to improve outcomes in this aggressive PCa subtype.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.