Paradoxical down-regulation of p16(INK4a) mRNA with advancing age in Acute Myeloid Leukemia

Hendrik J. M. de Jonge, Carolien M. Woolthuis, Eveline S. J. M. de Bont, Gerwin Huls*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

16 Citations (Scopus)
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Abstract

Aging is generally considered to be the consequence of stem cell attrition caused by the activity of tumor suppressor pathways that censor potentially malignant clones by eliciting apoptosis or senescence. An important effector of aging is the cyclin-dependent kinase inhibitor p16(INK4a), which is also a known suppressor of cancer. The expression of p16(INK4a) is very low or absent in young organisms but increases with advancing age. We recently showed that, unlike healthy cells, acute myeloid leukemia (AML) derived blasts show a down-regulation of p16(INK4a) mRNA with increasing age. Based on this observation we hypothesize that suppression of defense mechanisms which protect older cells against cellular and DNA damage might facilitate oncogenesis in older individuals.

Original languageEnglish
Pages (from-to)949-953
Number of pages5
JournalAging-Us
Volume1
Issue number11
DOIs
Publication statusPublished - Nov-2009

Keywords

  • p16(INK4a)
  • aging
  • Acute Myeloid Leukemia
  • senescence
  • HEMATOPOIETIC STEM-CELLS
  • SELF-RENEWAL
  • TUMOR-SUPPRESSOR
  • HEART-FAILURE
  • EXPRESSION
  • SENESCENCE
  • CANCER
  • GROWTH
  • BMI-1
  • OLDER

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