Biochemistry (Moscow)

, Volume 75, Issue 13, pp 1650–1666 | Cite as

Activated leukemic oncogenes AML1-ETO and c-kit: Role in development of acute myeloid leukemia and current approaches for their inhibition

  • A. V. RulinaEmail author
  • P. V. Spirin
  • V. S. Prassolov


Acute myeloid leukemia (AML) is a malignant blood disease caused by different mutations that enhance the pro-liferative activity and survival of blood cells and affect their differentiation and apoptosis. The most frequent disorders in AML are translocations between chromosomes 21 and 8 leading to production of a chimeric oncogene, AML1-ETO, and hyperexpression of the receptor tyrosine kinase KIT. Mutations in these genes often occur jointly. The presence in cells of two activated oncogenes is likely to trigger their malignization. The current approaches for treatment of oncologic diseases (bone marrow transplantation, radiotherapy, and chemotherapy) have significant shortcomings, and thus many laboratories are intensively developing new approaches against leukemias. Inhibiting expression of activated leukemic oncogenes based on the principle of RNA interference seems to be a promising approach in this field.

Key words

acute myeloid leukemia (AML) leukemic oncogenes AML1-ETO c-kit RNA interference 


Akt|a family of proteins playing an important role in intracellular signal transmission in mammals


acute myeloid leukemia


gene of Acute Myeloid Leukemia 1 encoding hemopoiesis-regulating protein


chimeric gene Acute Myeloid Leukemia 1-Eight-Twenty O ne


cis-acting siRNAs characteristic for plants


core-binding factor (heterodimeric transcription complex)


AML associated with disturbance in CBF function


ubiquitin E3 ligase


double-stranded RNA


extracellular-signal-regulated kinase


gene Eight-Twenty O ne


French-American-British classification of AML


fms-like receptor tyrosine kinase-3


gastrointestinal stromal tumor


histone deacetylase


feline sarcoma virus




Janus tyrosine kinase


juxtamembrane domain of receptor tyrosine kinase KIT


macrophage colony-stimulating factor


myelodysplastic syndrome




myeloproliferative diseases


messenger RNA


nuclear corepressor of transcription


Nervy protein homologous region


platelet-derived growth factor


phosphatidylinositol-3 kinase


RNAs interacting with PIWI proteins


proteins of Ago family (P-element Induced WImpy testis)


promyelocytic leukemia zinc finger (a transcription repressor)


posttranscriptional gene silencing


family of small GTPases involved in intracellular signal transmission


repeat-associated small interfering RNAs


RNA-dependent RNA polymerase


Runt protein homologous domain


RNA-induced silencing complex


RISC-loading complex


stem cell factor


Src family kinase


Src homology 2 domain

SHP-2 and SHP-3

Src homology region 2- and 3-domain phosphatase


small hairpin RNA


transcription corepressor


small interfering RNA


signal transducers and activator of transcription


vascular endothelial growth factor receptor


vesicular stomatitis virus G protein


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Copyright information

© Pleiades Publishing, Ltd. 2010

Authors and Affiliations

  • A. V. Rulina
    • 1
    Email author
  • P. V. Spirin
    • 1
  • V. S. Prassolov
    • 1
  1. 1.Engelhardt Institute of Molecular BiologyRussian Academy of SciencesMoscowRussia

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