• EGFR overexpression in OSCC drives tumor growth and metastasis, highlighting its potential as a therapeutic target. • TP53 mutations disrupt cell cycle regulation in OSCC, fueling oncogenesis and treatment resistance. • Dysregulation of the PI3K/AKT/mTOR pathway in OSCC promotes cell survival and proliferation. • Immunotherapy shows promise in OSCC, particularly in patients with high tumor mutational burden or PD-L1 expression. • Genetic profiling of OSCC tumors may guide personalized treatment strategies for improved patient outcomes.
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Patil et al. (2024) studied this question.
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