ArticleHuman mutation2026
Exploring the Role of
Article in Human mutation, 2026. 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
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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.
- Exploring the Role ofHuman mutation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Breast invasive carcinoma (BRCA) remains a leading cause of female cancer mortality, necessitating novel biomarkers and therapeutic targets. Heterogeneous nuclear ribonucleoprotein A3 (HNRNPA3) emerges as a potential regulator in tumor progression and immune modulation, yet its comprehensive role in BRCA remains uncharacterized. Methods: We conducted an integrated multiomics analysis of HNRNPA3 in BRCA using data from TCGA, GEO datasets, single-cell RNA sequencing, and spatial transcriptomics. Bioinformatics approaches included differential expression analysis, survival analysis, functional enrichment, immune microenvironment characterization, and drug sensitivity prediction. Results: HNRNPA3 was significantly upregulated in BRCA tissues and correlated with advanced tumor grade, metastasis, and poor prognosis across multiple cohorts. Functional enrichment revealed HNRNPA3's involvement in cell cycle regulation and immune-related pathways. Immune profiling demonstrated that high HNRNPA3 expression was associated with altered immune cell distribution, particularly CD4+ T cells, and reduced immunotherapy response. Spatial transcriptomics confirmed predominant HNRNPA3 expression in malignant regions. Drug sensitivity analysis identified potential therapeutic agents (CD-437 and talazoparib) targeting HNRNPA3-associated pathways. Conclusion: HNRNPA3 functions as a critical oncogenic regulator in BRCA by promoting tumor progression through cell cycle dysregulation and immune microenvironment remodeling. Its strong association with therapy resistance positions HNRNPA3 as both a prognostic biomarker and promising therapeutic target for breast cancer intervention strategies.
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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.