Table 2.

Key proteins and genes in head and neck cancer (HNC).

Key Protein/Gene	Role in Cancer	Clinical Relevance	Ref.
HPV E6/E7	HPV E6 inactivates p53 and HPV E7 inactivates Rb, leading to uncontrolled cell cycle progression and tumourigenesis.	HPV status is a critical prognostic marker and determines treatment strategies.	[33]
EGFR	Overexpressed in many HNCs, leading to increased cell proliferation.	Targeted by EGFR inhibitors like cetuximab, it predicts responsiveness to therapy.	[34]
TP53	Mutations lead to loss of tumour suppressor function, contributing to carcinogenesis.	Associated with poor prognosis and aggressive disease; potential target for therapy.	[35]
CDKN2A (p16)	Tumour suppressor gene, loss contributes to cell cycle deregulation.	Frequently mutated or deleted in HNC, indicative of poor prognosis.	[36]
PIK3CA	Mutation activates the PI3K/AKT pathway, promoting tumourigenesis.	Target for PI3K inhibitors associated with therapeutic resistance.	[37]
TIMPs (Tissue Inhibitors of Metalloproteinases)	Regulate ECM remodelling and metastasis by inhibiting MMPs, potentially suppressing tumour progression.	Targets for therapy and markers for disease progression and response to treatment.	[38]
Gal-3 (Galectin-3)	Involved in cell adhesion, migration, and tumour progression.	Potential marker for prognosis and therapeutic targeting.	[39]
MMPs (Matrix Metalloproteinases)	Facilitate tumour invasion and metastasis through ECM degradation.	Biomarkers for invasive potential and therapeutic targets.	[40]
Fibronectin	Contributes to cell adhesion and migration, influencing tumour growth and metastasis.	Insights into tumour progression and potential therapeutic implications.	[41]