The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior

Cell Cycle. 2009 Oct 1;8(19):3120-4. doi: 10.4161/cc.8.19.9627.


In response to diverse stresses, the tumor suppressor p53 differentially regulates its target genes, variably inducing cell-cycle arrest, apoptosis or senescence. Emerging evidence indicates that p53 plays an important role in regulating hematopoietic stem cell (HSC) quiescence, self-renewal, apoptosis and aging. The p53 pathway is activated by DNA damage, defects in ribosome biogenesis, oxidative stress and oncogene induced p19 ARF upregulation. We present an overview of the current state of knowledge about p53 (and its target genes) in regulating HSC behavior, with the hope that understanding the molecular mechanisms that control p53 activity in HSCs and how p53 mutations affect its role in these events may facilitate the development of therapeutic strategies for eliminating leukemia (and cancer) propagating cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Apoptosis
  • Cell Cycle
  • Cellular Senescence
  • DNA Damage
  • Hematopoietic Stem Cells / cytology*
  • Hematopoietic Stem Cells / physiology
  • Proto-Oncogene Proteins c-mdm2 / metabolism
  • Transcription Factors / metabolism
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Protein p53 / physiology*


  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Proto-Oncogene Proteins c-mdm2