Research Progress of A20 in Acute Leukemia

Acute leukemia (AL) is a malignant tumor originating from hematopoietic stem cells. Its outstanding feature is the abnormal proliferation and aggregation of clonal leukemia cells in bone marrow and other hematopoietic tissues. Although chemotherapy, targeted immunotherapy and hematopoietic stem cell transplantation have been widely used in clinic, there are still relapse and refractory cases in AL patients. Finding new therapeutic targets and screening prognostic molecules are of great significance for the treatment and prognosis of AL. A20 protein, also known as tumor necrosis factor α-induced protein 3 (TNFAIP3), is a key protein that negatively inhibits the activation of nuclear transcription factor kB (NF-κB) and plays an important role in anti-tumor immune and inflammatory response. In leukemia and lymphoma, A20 is often inactivated, mutated or deleted. Lack of A20 can significantly inhibit the surveillance function of immune cells and mediate tumor immune escape. Therefore, exploring the mechanism of A20 in AL may have important research value and clinical significance for the treatment of AL. The purpose of this paper is to review the research progress of A20 in acute leukemia, and provide new theoretical basis and reference value for the pathogenesis research and targeted therapy of leukemia.