Author: Tanusree Naskar
DOI Link: https://doi.org/10.70798/Bijmrd/02080022
ABSTRACT: Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by clonal expansion of myeloid progenitor cells, impaired differentiation, and aberrant proliferation. Transcription factors play a pivotal role in governing hematopoietic lineage commitment, differentiation, and survival, and their dysregulation is central to AML pathogenesis. Key transcription factors implicated in AML include PU.1, C/EBPα, RUNX1, GATA2, and AML1-ETO fusion proteins, each orchestrating distinct but interconnected signaling networks. Alterations in transcription factor expression or activity, often via mutations, epigenetic modifications, or signaling pathway deregulation, contribute to leukemogenesis, chemoresistance, and poor prognosis. This review highlights current knowledge on the regulation of transcription factors in AML, including upstream modulators, downstream targets, and cross-talk with oncogenic pathways. Additionally, it discusses experimental insights from AML cell lines, patient-derived xenografts, and clinical samples, with a focus on translational approaches targeting transcription factor networks. Understanding the molecular regulation of transcription factors in AML offers opportunities for novel therapeutic interventions, including small molecule inhibitors, epigenetic modulators, and targeted combination therapies.
Keywords: AML, Transcription factors, PU.1, C/EBPα, RUNX1, GATA2, AML1-ETO, Epigenetic Regulation, Therapeutic Targets.
Page No: 193-200