ArticleDiscover oncology2025
Causal role of immune cells in head and neck squamous cell carcinoma.
Article in Discover oncology, 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
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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.
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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.
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Who cites it
1 citing paper in PubMed.
- B Cell dysfunction in tumor-draining lymph nodes predicts relapse in oral squamous cell carcinoma.Cancer immunology, immunotherapy : CII · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Chronic inflammation, immune cell infiltration, and metabolic reprogramming play a crucial role in the development of head and neck squamous cell carcinoma (HNSCC). Based on the summary-level data from a genome-wide association study (GWAS), this study used Mendelian randomization (MR) analysis to investigate the causal relationship between immune cell phenotype and HNSCC. Two-step MR was employed to quantify the proportion of the effect of metabolite-mediated immunophenotypes on HNSCC. 16 immune phenotypes exhibited a causal relationship with HNSCC. HLA DR + CD4 + AC (OR: 1.31, 95% CI 1.07-1.59, P < 0.01) and EM CD8br AC cells (OR: 1.36, 95% CI 1.14-1.62, P < 0.01) showed the most significant P values. 13 metabolites have a causal relationship with HNSCC (P < 0.05). The proportion of the effect of Bilirubin degradation product, C16H18N2O5 (3) levels-mediated HLA DR + CD4 + AC on HNSCC was 7.17% (95% CI 1.04%-13.3%), while the proportion of the effect of Glutamine to alanine ratio-mediated EM CD8br AC on HNSCC was 8.88% (95% CI 2.2%-15.6%). Moreover, single-cell RNA-sequencing analysis confirmed that HLA DR + CD4 + AC and EM CD8br AC cells were commonly present in the HNSCC tumor microenvironment (TME). High expression of two immune phenotypes indicated a poorer prognosis. The results of differentially expressed genes (DEGs) analysis and functional enrichment indicated that Interferon-induced protein with tetratricopeptide repeats 1 (IFIT1)/Follicular dendritic cell secreted protein (FDCSP) and Keratin 19 type I (KRT19)/Kallikrein-related peptidase 5 (KLK5) may be responsible genes for two immune phenotypes, respectively. The results of quantitative real-time polymerase chain reaction (qRT-PCR) and survival analysis showed that FDCSP was significantly downregulated in HNSCC and could exert a protective effect. Collectively, our study clarified the causal relationship between immune cells, metabolites, and HNSCC, providing new insight for clinical diagnosis and treatment of HNSCC.
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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.