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Cancer-Critical Genes I: Proto-oncogenes01:33

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Updated: Oct 4, 2025

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
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An oncogenic enhancer encodes selective selenium dependency in AML.

Kenneth Eagle1, Yajian Jiang2, Xiangguo Shi3

  • 1Department of Molecular and Human Genetics, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA; Program in Quantitative and Computational Biosciences, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.

Cell Stem Cell
|February 2, 2022
PubMed
Summary
This summary is machine-generated.

Researchers identified a MYB-regulated enhancer that upregulates SEPHS2, a gene crucial for acute myeloid leukemia (AML) cell survival. Targeting selenoprotein production, including SEPHS2, shows promise as a therapeutic strategy for AML.

Keywords:
AMLMYBSEPHS2enhancerhematopoiesishematopoietic stem cellleukemia stem cellseleniumselenocysteine

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Transcriptional deregulation is a key feature of acute myeloid leukemia (AML), driving cancer-specific expression patterns.
  • Identifying unique vulnerabilities in AML is crucial for developing targeted therapies.

Purpose of the Study:

  • To identify novel, actionable therapeutic targets in AML by integrating enhancer landscapes with genetic dependency data.
  • To investigate the role of a specific MYB-regulated enhancer and its downstream gene, SEPHS2, in AML pathogenesis.

Main Methods:

  • Integrated pan-cancer enhancer mapping with genetic dependency profiling.
  • Utilized patient-derived samples and mouse models to study gene regulation and function.
  • Performed SEPHS2 knockout studies and selenium dietary restriction experiments.

Main Results:

  • Discovered an AML-enriched enhancer regulated by MYB, which controls SEPHS2 expression.
  • Demonstrated that SEPHS2 upregulation promotes antioxidant function essential for AML cell survival.
  • Showed that SEPHS2 and selenoprotein pathway genes are vital for AML growth in vitro and in vivo.
  • Found that SEPHS2 inhibition or selenium restriction delays leukemogenesis with minimal impact on normal hematopoiesis.

Conclusions:

  • Enhancer mapping is a valuable tool for identifying selective cancer dependencies.
  • The selenoprotein production pathway, regulated by SEPHS2, represents a promising therapeutic target for AML.