ArticleNature communications2024
Hallmarks of a genomically distinct subclass of head and neck cancer.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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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
20 citing papers in PubMed.
- Melanoma evolution in the lymph node shapes systemic outcomes.bioRxiv : the preprint server for biology · 2026Article
- Spatially defined microenvironmental niches are associated with clinical outcome and tumor ecosystem diversity in head and neck cancer.Med (New York, N.Y.) · 2026Article
- Review
- Association Between the Dietary Inflammatory Index (DII) and Head and Neck Cancer Incidence-A Narrative Review.Nutrients · 2026Review
- Genetics and Molecular Mechanisms in Oral Squamous Cell Carcinoma: A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- The Silent Link: Exploring the Impact of Periodontal Diseases on Head and Neck Carcinogenesis.Clinical and experimental dental research · 2026Review
- Sex-based immune differences influence tumor progression in head and neck squamous cell carcinoma.Oral oncology · 2026Article
- TMEM92 drives EMT-associated invasiveness, cisplatin resistance, and immune suppression in head and neck squamous cell carcinoma.Scientific reports · 2026Article
- N4BP1 is essential for the development of oral cancer via controlling both cancer cells and immune microenvironment.Cell death & disease · 2026Article
- Methotrexate-triggered ferroptosis suppresses oral cancer progression by phosphorylated KEAP1-mediated NRF2 degradation to inhibit SLC7A11/GPX4 signaling pathway.Cancer cell international · 2026Article
- Genomic Profiling of Laryngeal Squamous Cell Carcinoma Reveals Novel Biomarkers for Precision Medicine.Journal of personalized medicine · 2025Article
- Comparative Analysis Reveals Recurrent Molecular Alterations in Low-Risk Human Papillomavirus 6 and Human Papillomavirus 11-Associated Squamous Cell Carcinoma of the Uterine Cervix and Vulva.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2025Article
- Dual CDK and MEK Inhibition potentiates CD8Journal of experimental & clinical cancer research : CR · 2025Article
- New insights into the genetic progression of cancer through longitudinal analysis of oral lesions.The Journal of pathology · 2025Article
- Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025Review
- LINC01518 functions as an oncogene in head and neck squamous cell carcinoma (HNSCC) by modulating miR-1-3p/Slug and miR-216b-5p/GRP78 axis.Scientific reports · 2025Article
- Extracellular vesicles in head and neck cancer: mediators of oncogenesis, immune evasion, and therapy resistance.Frontiers in immunology · 2025Review
- Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment.Frontiers in immunology · 2025Review
- Article
- Hallmarks of a genomically distinct subclass of head and neck cancer.Nature communications · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is caused by an accumulation of somatic mutations and copy number alterations (CNAs). Besides mutations, these copy number changes are key characteristics of cancer development. Nonetheless, some tumors show hardly any CNAs, a remarkable phenomenon in oncogenesis. Head and neck squamous cell carcinomas (HNSCCs) arise by either exposure to carcinogens, or infection with the human papillomavirus (HPV). HPV-negative HNSCCs are generally characterized by many CNAs and frequent mutations in CDKN2A, TP53, FAT1, and NOTCH1. Here, we present the hallmarks of the distinct subgroup of HPV-negative HNSCC with no or few CNAs (CNA-quiet) by genetic profiling of 802 oral cavity squamous cell carcinomas (OCSCCs). In total, 73 OCSCC (9.1%) are classified as CNA-quiet and 729 as CNA-other. The CNA-quiet group is characterized by wild-type TP53, frequent CASP8 and HRAS mutations, and a less immunosuppressed tumor immune microenvironment with lower density of regulatory T cells. Patients with CNA-quiet OCSCC are older, more often women, less frequently current smokers, and have a better 5-year overall survival compared to CNA-other OCSCC. This study demonstrates that CNA-quiet OCSCC should be considered as a distinct, clinically relevant subclass. Given the clinical characteristics, the patient group with these tumors will rapidly increase in the aging population.
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