Evidence map›Paper›PMID 42490773›Full record

ArticleWorld journal of oncology2026

Integrated Transcriptomic Analysis Identifies Potential Biomarkers in Castration-Resistant Prostate Cancer.

Abdulghani A Naeem, Saud A Abdulsamad, Ateequllah Hayat, Ayesha Naeem, Nada Alhazmi, Ghaith Fallata, Anas Bokhari, Abdulmajeed H Alharbi, Kinani A Alkinani, Abdullah M Alshehri and 1 more

Abstract read
In one paragraph

Article in World journal of oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Abdulghani A NaeemDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Saud A AbdulsamadDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Ateequllah HayatDepartment of Molecular and Biomedical Sciences, City St George's, University of London, London, UK.
Ayesha NaeemDepartment of Molecular and Biomedical Sciences, City St George's, University of London, London, UK.
Nada AlhazmiDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Ghaith FallataDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Anas BokhariDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Abdulmajeed H AlharbiDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Kinani A AlkinaniDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Abdullah M AlshehriDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah 21423, Saudi Arabia.
Khadijah M AldabbaghKing Abdullah International Medical Research Center (KAIMRC), Jeddah 21423, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Castration-resistant prostate cancer (CRPC) represents an aggressive stage of prostate cancer that develops following resistance to androgen deprivation therapy. Although androgen receptor (AR) signaling remains a central driver of disease progression, additional adaptive molecular mechanisms contribute to therapeutic resistance. Understanding the transcriptional programs underlying CRPC may facilitate the identification of novel biomarkers and therapeutic targets. Methods: RNA sequencing-based transcriptomic profiling was performed to compare a non-malignant prostate epithelial model (PNT2) with a CRPC model retaining AR expression (22Rv1). Differential gene expression analysis was conducted using DESeq2. Functional enrichment analyses were performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Gene co-expression network analysis was applied to identify coordinated regulatory interactions. Clinical validation of candidate genes was performed using Gene Expression Profiling Interactive Analysis 2 (GEPIA2), integrating datasets from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) project. Results: Transcriptomic comparison revealed extensive transcriptional remodeling associated with the castration-resistant phenotype. Several genes, including Conclusions: Integrated transcriptomic and network analyses reveal coordinated metabolic, epigenetic, and DNA damage response pathways contributing to CRPC progression and identify potential combinatorial therapeutic vulnerabilities in advanced prostate cancer.

Indexed as

BioinformaticsBiomarkersCastration-resistant prostate cancerGene expressionProstate cancerRNA sequencing

Identifiers

PMID42490773
PMCPMC13375418

What Socratic 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 Socratic graph.