ReviewBiomedicines2026
Metabolism and Metabolic Reprogramming in Laryngeal Squamous Cell Carcinoma.
Review in Biomedicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Resistance-oriented immunometabolic circuits in laryngeal squamous cell carcinoma: glycolysis-lactate signaling, mitochondrial stress, and tumor-myeloid crosstalk.Frontiers in immunology · 2026Review
- YWHAG overexpression correlates with an immune-desert microenvironment and poor prognosis in laryngeal squamous cell carcinoma.Frontiers in immunology · 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
Laryngeal squamous cell carcinoma (LSCC) remains a major clinical challenge within head and neck oncology, with five-year survival rates showing minimal improvement over recent decades despite advances in surgical and multimodal therapeutic strategies. Increasing evidence identifies metabolic reprogramming as a central driver of tumor progression, therapeutic resistance, and immune evasion in LSCC. Beyond the classical Warburg effect, LSCC exhibits profound metabolic reprogramming, involving coordinated alterations in carbohydrate, amino acid, lipid, and iron metabolism that support adaptation to hypoxic and nutrient-deprived microenvironments. Hypoxia-inducible factors, particularly HIF-1α, coordinate these key biochemical pathways and enzymatic steps by integrating glycolysis, glutaminolysis, folate-dependent one-carbon pathways, lipid synthesis, and mitochondrial remodeling, while also influencing stromal and immune components of the tumor microenvironment. Metabolic crosstalk between tumor cells, cancer-associated fibroblasts, and immune populations promotes immunosuppression through nutrient competition and accumulation of metabolites such as lactate and lipid-derived mediators. In parallel, dysregulated iron handling and altered ferroptosis susceptibility emerge as key determinants of tumor aggressiveness and treatment response. This review synthesizes current evidence on metabolic rewiring in laryngeal squamous cell carcinoma, highlighting how alterations in metabolic pathways create targetable vulnerabilities that drive tumor biology, immune modulation, and resistance to conventional and emerging therapies. Elucidating these metabolic dependencies may support the development of metabolism-based biomarkers and therapeutic strategies in laryngeal squamous cell carcinoma, providing an integrated and translational perspective that links tumor metabolism with microenvironmental interactions and immune modulation, while highlights emerging therapeutic vulnerabilities.
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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.