Tumor protein 53 mutations in acute myeloid leukemia: conventional induction chemotherapy or novel therapeutics.

摘要: Purpose of review Tumor protein 53 (TP53) is involved in fundamental processes cancer, aging, and DNA repair. Thus, TP53 dysfunction implicated malignant remains the most commonly mutated gene cancer but represents a relatively small proportion acute myeloid leukemia (AML). Patients with TP53-mutated AML attain inferior responses to therapy resulting poor overall outcomes. Recent findings Traditional treatment approaches conventional chemotherapy yields suboptimal for patients mutant compared wildtype TP53. In recent years, there increasing interest understanding role underlying biology mutations efforts harness physiological tumor suppressive function protein. Novel combination targeted therapies may contribute improved outcomes; however, be short-lived ongoing research indicated evaluate relapse-risk reduction strategies. These benefit from consideration enrollment clinical trials or lower intensity lieu intensive chemotherapy. Summary Pharmacological treatments targeting pathway addition novel emerging therapeutics immunotherapy-based hold promise AML.