DefinePK

Abstract

Oral squamous cell carcinoma (OSCC) represents a significant global health burden, marked by high mortality and poor prognosis. It is most commonly observed in individuals who consume tobacco, particularly long-term users. The disease arises from a series of cellular and molecular changes, including alterations in gene expression that drive cancer development. Understanding and potentially reversing these genetic and epigenetic changes may aid in disease prevention and treatment.
Among the key molecular aberrations involved in OSCC pathogenesis are alterations in the CDKN2A gene. Located on chromosome 9p21, CDKN2A encodes two critical tumor suppressor proteins—p16^INK4a^ and p14^ARF^—which regulate the cell cycle and apoptosis, respectively. Loss of function in CDKN2A disrupts these regulatory processes, thereby promoting cancer development.
This review explores the molecular biology of CDKN2A, its alterations in OSCC, the associated signaling pathways, and potential therapeutic implications. Epigenetic and genetic regulation of CDKN2A may offer promising strategies for cancer prevention and therapy. Ongoing research into this gene and its related pathways holds the potential to deliver transformative insights, ultimately improving prognostic accuracy and treatment outcomes for OSCC patients