Answers are grounded in this paper and cite their sources.
Integrated analyses reveal decreased oncogenic drivers and inflammatory signalling in HPV-positive HNSCC, suggesting better prognosis.
Head and neck squamous cell carcinoma (HNSCC) is a significant global health concern. Though tobacco, alcohol, and betel quid have been previously recognized as the main risk factors for a long time, unique cases of human papillomavirus (HPV) infection-mediated cancer are now a very emerging topic of discussion. HPV-mediated tumors show distinct biological and clinical properties. Interestingly, it has been observed that though HPV-positive HNSCC often is the sole cause for advanced-stage cancers, patients still have far better initial survival outcomes than those with HPV-negative disease. To better understand this paradox, we carried out integrated transcriptomic and epigenomic analyses using TCGA and other publicly available datasets. Our results depict that HPV-positive tumors suppress some key oncogenic drivers, such as MMP1, MMP11, PTHLH, and SPRR2G, along with some very important pro-inflammatory cytokines like IL1?, IL1?, and TNF. Whereas, all of these genes have many-fold higher expression in the HPV-negative scenario. This change in gene expression profile weakens pathways involved in invasion, extracellular matrix remodeling, and chronic inflammation, ultimately creating a less aggressive tumor environment in HPV-positive HNSCC. On a mechanistic level, we observed HPV-positive cells modulating havoc in chromatin regulation. Specifically, they lose H3K27ac and replace RELA binding with p63 at various pro-inflammatory cytokine promoters, shifting the transcriptional control toward epithelial survival pathways. This duality—reduced inflammatory signalling along with reinforced epithelial persistence—helps to understand why HPV-positive tumors are associated with a more favorable prognosis. In summary, our study establishes HPV-positive HNSCC as biologically different cancer types shaped by viral regulation of chromatin, transcription factors, and immune signalling, offering altogether a new insight into the unique clinical outcomes.
No takes yet. Share an insight, caveat, or question.
Mondal et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: