ArticleCancer cell international2025
Aldolase a in pan-cancer and lung squamous cell carcinoma: prognostic value and macrophage-driven immune suppression unveiled by multi-omics and cohort validation.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
backgroundAldolase A (ALDOA), a key glycolytic enzyme, has been implicated in tumor progression and metabolic reprogramming across multiple cancers [1]. However, its role in lung squamous cell carcinoma (LUSC) remains largely unexplored. Recent studies suggest that ALDOA may influence the tumor immune microenvironment, particularly through its association with macrophages [2, 3]. This study aims to investigate the prognostic value of ALDOA in LUSC and its role in macrophage-mediated immune suppression.
methodsWe conducted a comprehensive pan-cancer analysis to evaluate ALDOA expression, genomic alterations, and prognostic relevance across different cancer types. In LUSC, we validated its prognostic value using immunohistochemical (IHC) staining and independent patient cohorts. Immune infiltration was assessed using multiple bioinformatics algorithms and single-cell RNA sequencing (scRNA-seq) from the TISCH2 database. Spatial transcriptomics and immunofluorescence (IF) staining were performed to determine ALDOA's co-localization with CD68 + macrophages in LUSC tissues. Functional enrichment and drug sensitivity analyses were conducted to explore ALDOA's role in tumor progression and therapeutic resistance.
resultsALDOA was significantly overexpressed in multiple cancers, with LUSC showing one of the highest expression levels. Elevated ALDOA expression was strongly correlated with poor overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) in LUSC patients. Copy number variations and promoter hypomethylation were identified as potential mechanisms driving ALDOA overexpression. ALDOA-high tumors exhibited increased M0 macrophage and reduced CD8 + T-cell infiltration, suggesting a role in immune suppression and evasion. Spatial transcriptomic and immunofluorescence analyses confirmed the co-localization of ALDOA with CD68 + tumor-associated macrophages (TAMs). Additionally, ALDOA-high tumors demonstrated increased resistance to multiple chemotherapeutic agents and EGFR-TKIs, highlighting its potential as a predictive biomarker for drug response.
conclusionOur findings establish ALDOA as a robust prognostic biomarker and a key regulator of macrophage-mediated immune suppression in LUSC. Its involvement in tumor metabolism, immune evasion, and therapy resistance suggests that targeting ALDOA could enhance both metabolic inhibition strategies and immune checkpoint blockade therapies. Future research should focus on mechanistic studies and therapeutic interventions targeting ALDOA to improve treatment outcomes in LUSC.
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.