ArticleTranslational cancer research2026
A pan-cancer functional atlas of ADH1A reveals its conserved role in the tumor microenvironment and immunity.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: The human alcohol dehydrogenase (ADH) gene family is increasingly implicated in tumorigenesis, yet the roles of ADH1A across diverse solid tumors remain largely uncharacterized. This study aimed to explore the expression landscape, regulatory networks, and conserved biological functions of ADH1A through a pan-cancer analysis. Methods: We analyzed ADH1A expression across solid tumors using integrated The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) transcriptomic data, with protein-level validation from the Human Protein Atlas, 36 paired human tumor-normal tissues, and multiple tissues from BALB/c mice. To characterize ADH1A-associated biological contexts, we performed differential expression, co-expression, principal component, enrichment, and network analyses, together with survival and immune infiltration analyses. Results: ADH1A was significantly downregulated in most solid tumors relative to their normal counterparts, suggesting its potential diagnostic value. Co-expression network analysis identified that ADH1A was associated with angiogenesis, cell adhesion, and leukocyte migration, implicating its potential association with the tumor microenvironment and providing a rationale for future investigation into its potential predictive value for immunotherapy. We constructed a putative upstream regulatory network, including transcription factors and microRNAs, and a downstream protein interaction network for ADH1A based on integrative bioinformatics predictions. Notably, differential analysis suggested potential functional divergence of ADH1A between lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Furthermore, our cross-species comparison reveals both conserved and divergent ADH1A expression between humans and BALB/c mice, providing a partial contextual baseline for future preclinical studies. Conclusions: Our findings suggest ADH1A may serve as a potential diagnostic and prognostic biomarker across various solid tumors. By mapping its functional and regulatory landscape, this work provides a new rationale for investigating ADH1A as a candidate predictive biomarker for immunotherapy and uncovers novel avenues for exploring its biological mechanisms in cancer.
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