Abstract
P53 is a crucial tumor suppressor gene that plays an essential role in maintaining genomic stability, regulating cell cycle progression, and inducing apoptosis. In hematologic malignancies, P53 mutations are frequently associated with poor prognosis, treatment resistance, and immune evasion. Recent research has highlighted the impact of P53 dysfunction on tumor immune escape mechanisms, including impaired antigen presentation, altered cytokine signaling, and recruitment of immunosuppressive cells. This review integrates recent findings on P53 mutations in hematologic malignancies, focusing on their role in immune evasion and potential therapeutic strategies aimed at restoring P53 function or targeting associated pathways. Understanding these mechanisms may provide new insights into the development of effective immunotherapeutic approaches for hematologic cancers.