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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Related Experiment Video

Updated: Nov 19, 2025

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Inflammation-driven deaminase deregulation fuels human pre-leukemia stem cell evolution.

Qingfei Jiang1, Jane Isquith1, Luisa Ladel1

  • 1Division of Regenerative Medicine, Department of Medicine, Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093-0820, USA.

Cell Reports
|January 27, 2021
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Inflammation drives leukemia stem cell (LSC) evolution through APOBEC3C-induced proliferation and ADAR1-mediated splicing changes. This study elucidates these key mechanisms in pre-leukemia stem cell progression.

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Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells
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Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Inflammation-associated base deaminases contribute to therapeutic resistance in cancers.
  • The specific role of these enzymes in the evolution of pre-leukemia stem cells (pre-LSCs) to acute myeloid leukemia stem cells (LSCs) remains unclear.

Purpose of the Study:

  • To investigate the role of APOBEC3C and ADAR1 in the progression of pre-LSCs to LSCs.
  • To identify the molecular mechanisms driving this evolution in myeloproliferative neoplasms (MPNs).

Main Methods:

  • Comparative whole-genome and whole-transcriptome sequencing of FACS-purified pre-LSCs from MPN patients.
  • Lentiviral overexpression of APOBEC3C and knockdown of ADAR1.
  • JAK2/STAT3 inhibition using ruxolitinib or fedratinib.

Main Results:

  • APOBEC3C upregulation, increased C-to-T mutations, and HSPC proliferation were observed during pre-LSC to LSC progression.
  • Inflammatory splice isoform overexpression and ADAR1p150-induced RNA editing correlate with APOBEC3C upregulation.
  • STAT3 editing, STAT3β isoform switching, and elevated phospho-STAT3 characterize LSC evolution, preventable by JAK2/STAT3 inhibition or ADAR1 knockdown.

Conclusions:

  • Primate-specific APOBEC3C drives pre-LSC proliferation and contributes to LSC evolution.
  • ADAR1-mediated splicing deregulation is a critical factor in pre-LSC to LSC transformation.
  • Targeting APOBEC3C and ADAR1 pathways may offer therapeutic strategies for MPNs and AML.