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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
Review

Abstract

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 

Abbreviations

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

AML

acute myeloid leukemia

AML1

gene of Acute Myeloid Leukemia 1 encoding hemopoiesis-regulating protein

AML1-ETO

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

casiRNA

cis-acting siRNAs characteristic for plants

CBF

core-binding factor (heterodimeric transcription complex)

CBF AML

AML associated with disturbance in CBF function

Cbl

ubiquitin E3 ligase

dsRNA

double-stranded RNA

ERK

extracellular-signal-regulated kinase

ETO

gene Eight-Twenty O ne

FAB

French-American-British classification of AML

FLT-3

fms-like receptor tyrosine kinase-3

GIST

gastrointestinal stromal tumor

HDAC

histone deacetylase

HZ4-FeSV

feline sarcoma virus

IL

interleukin

JAK

Janus tyrosine kinase

JM-domain

juxtamembrane domain of receptor tyrosine kinase KIT

M-CSF

macrophage colony-stimulating factor

MDS

myelodysplastic syndrome

miRNA

microRNA

MPD

myeloproliferative diseases

mRNA

messenger RNA

N-CoR

nuclear corepressor of transcription

NHR

Nervy protein homologous region

PDGF

platelet-derived growth factor

PI3K

phosphatidylinositol-3 kinase

piRNA

RNAs interacting with PIWI proteins

PIWI

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

PLZF

promyelocytic leukemia zinc finger (a transcription repressor)

PTGS

posttranscriptional gene silencing

Ras

family of small GTPases involved in intracellular signal transmission

rasiRNA

repeat-associated small interfering RNAs

RdRP

RNA-dependent RNA polymerase

RHD

Runt protein homologous domain

RISC

RNA-induced silencing complex

RLC

RISC-loading complex

SCF

stem cell factor

SFK

Src family kinase

SH2

Src homology 2 domain

SHP-2 and SHP-3

Src homology region 2- and 3-domain phosphatase

shRNA

small hairpin RNA

Sin3

transcription corepressor

siRNA

small interfering RNA

STAT

signal transducers and activator of transcription

VEGFR

vascular endothelial growth factor receptor

VSV-G

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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