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

被引:24
|
作者
Rulina, A. V. [1 ]
Spirin, P. V. [1 ]
Prassolov, V. S. [1 ]
机构
[1] Russian Acad Sci, VA Engelhardt Mol Biol Inst, Moscow 119991, Russia
关键词
acute myeloid leukemia (AML); leukemic oncogenes; AML1-ETO; c-kit; RNA interference; RECEPTOR TYROSINE KINASE; STEM-CELL FACTOR; CORE-BINDING-FACTOR; RISK MYELODYSPLASTIC SYNDROME; DOUBLE-STRANDED-RNA; TRANSCRIPTION-FACTOR; IMATINIB MESYLATE; GROWTH-FACTOR; ZINC-FINGER; PROMYELOCYTIC LEUKEMIA;
D O I
10.1134/S0006297910130092
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1650 / 1666
页数:17
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