Rational targeting in acute promyelocytic leukemia

Nikolaos A. Papanikolaou

Research output: Contribution to journalArticlepeer-review


Acute promyelocytic leukemia (ARL) is characterized by the nearly homogeneous expression of the fusion oncogenic protein PML-RARα and the testis-specific cyclin A1 protein, which are implicated in its pathogenesis. PML-RARα binds all-trans retinoic acid with high affinity inducing granulocytic differentiation and remission. Current approaches with high doses of single or combined all-trans retinoic acid and chemotherapeutic agents, though relatively efficacious in the beginning, are highly toxic with severe side-effects (retinoic acid syndrome) and are followed by relapse in a high proportion of patients. Here it is proposed that targeting APL with low levels of all-trans retinoic acid combined with small molecule inhibitors of cyclin-dependent kinases may have the potential to be equally or more efficacious as any of the current single or combined agent approaches, affording reduced toxicity and relapse rates.

Original languageEnglish (US)
Pages (from-to)21-27
Number of pages7
JournalIn vivo (Athens, Greece)
Issue number1
StatePublished - Jan 2010
Externally publishedYes


  • Acute myeloid leukemia (AML)
  • Acute promyelocytic leukemia (APL)
  • All-trans retinoic acid (ATRA)
  • CCAAT/enhancer binding protein epsilon (C/EBPε)
  • Cell cycle arrest
  • Cyclin A1
  • Cyclin A2 (A2)
  • Cyclin dependent-kinase 1 (CDK1)
  • Cyclin dependent-kinase 2 (CDK2)
  • Differentiation
  • Granulocyte
  • PML-RARα
  • Promyelocyte (PM)
  • Promyelocytic leukemia zinc finger protein (PLZF)
  • Retinoic acid receptor α (RARα)
  • Rexinoid acid receptor (RXR)

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology


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