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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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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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Related Experiment Video

Updated: Apr 5, 2026

Efficient Purification and LC-MS/MS-based Assay Development for Ten-Eleven Translocation-2 5-Methylcytosine Dioxygenase
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[TET2 as a gatekeeper for hematologic malignancies].

Hideharu Muto1, Mamiko Sakata-Yanagimoto, Shigeru Chiba

  • 1Department of Hematology, Faculty of Medicine, University of Tsukuba.

[Rinsho Ketsueki] the Japanese Journal of Clinical Hematology
|August 11, 2015
PubMed
Summary
This summary is machine-generated.

Ten Eleven Translocation 2 (TET2) mutations are linked to blood cancers. TET2 acts as a gatekeeper, preventing hematopoietic stem cells from becoming malignant.

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Hematology

Background:

  • Ten Eleven Translocation (TET) family proteins are dioxygenases crucial for DNA demethylation.
  • TET2 mutations are prevalent in various myeloid malignancies and T-cell lymphomas.

Purpose of the Study:

  • To investigate the role of TET2 in hematopoietic stem cell function and the development of hematologic malignancies.
  • To explore the implications of TET2 mutations in pre-cancerous states.

Main Methods:

  • Generation and analysis of Tet2 knockout/knockdown mouse models.
  • Assessment of hematopoietic stem cell self-renewal and competitive repopulation capacity.
  • Correlation analysis with TET2 mutation frequencies in human populations.

Main Results:

  • Tet2 mutations enhance hematopoietic stem cell self-renewal and repopulation.
  • Tet2-deficient mice develop myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), and T-cell lymphomas.
  • TET2 mutations are found in a notable percentage of healthy elderly individuals, suggesting a pre-malignant state.

Conclusions:

  • TET2 plays a critical gatekeeper role in hematopoietic stem/progenitor cells.
  • Loss of TET2 function predisposes cells to hematologic malignancies through additional genetic mutations.
  • TET2 is a key regulator preventing the development of blood cancers.