2. Academic Validation
  3. TET2 mutation in acute myeloid leukemia: biology, clinical significance, and therapeutic insights

TET2 mutation in acute myeloid leukemia: biology, clinical significance, and therapeutic insights

  • Clin Epigenetics. 2024 Nov 9;16(1):155. doi: 10.1186/s13148-024-01771-2.
Qiang Gao 1 2,  Kefeng Shen 3 4,  Min Xiao 5 6
Affiliations

Affiliations

  • 1 Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
  • 2 Immunotherapy Research Center for Hematologic Diseases of Hubei Province, Wuhan, 430030, Hubei, China.
  • 3 Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. [email protected].
  • 4 Immunotherapy Research Center for Hematologic Diseases of Hubei Province, Wuhan, 430030, Hubei, China. [email protected].
  • 5 Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. [email protected].
  • 6 Immunotherapy Research Center for Hematologic Diseases of Hubei Province, Wuhan, 430030, Hubei, China. [email protected].
PMID: 39521964 DOI: 10.1186/s13148-024-01771-2
Abstract

TET2 is a critical gene that regulates DNA methylation, encoding a dioxygenase protein that plays a vital role in the regulation of genomic methylation and Other epigenetic modifications, as well as in hematopoiesis. Mutations in TET2 are present in 7%-28% of adult acute myeloid leukemia (AML) patients. Despite this, the precise mechanisms by which TET2 mutations contribute to malignant transformation and how these insights can be leveraged to enhance treatment strategies for AML patients with TET2 mutations remain unclear. In this review, we provide an overview of the functions of TET2, the effects of its mutations, its role in clonal hematopoiesis, and the possible mechanisms of leukemogenesis. Additionally, we explore the mutational landscape across different AML subtypes and present recent promising preclinical research findings.

Keywords

TET2; Acute myeloid leukemia; DNA methylation; Mechanisms; Therapeutic insights.

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