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Key molecular mechanisms associated with cell malignant transformation in acute myeloid leukemia

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Abstract

Cancer, along with cardiovascular disorders, is one of the most important problems of healthcare. Pathologies of the hematopoietic system are the most prevalent in patients under 30 years of age, including acute myeloid leukemia (AML), which is widespread and difficult to treat. The review considers the mechanisms that play a significant role in AML cell malignant transformation and shows the contributions of certain genes to both remission and resistance of AML cells to various treatments.

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Abbreviations

AML:

acute myeloid leukemia

Bcl-2:

B-cell lymphoma 2

Bcl-xL:

B-cell lymphoma-extra large

FLT-3:

fmsrelated tyrosine kinase 3

Mcl-2:

myeloid leukemia cell differentiation protein 2

XP:

xeroderma pigmentosum

XPA–F:

XP complementation groups A–F

ERCC1:

excision repair crosscomplementing group 1

Hh:

hedgehog genes

Ptc:

Patched

Gli1–3:

hlioma-associated oncogene homologs 1–3

JNK:

c-Jun N-terminal kinase

MAPK:

mitogen-activated protein kinase

Bcr-Abl:

breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1

BER:

base excision repair

NER:

nucleotide excision repair

MMR:

mismatch repair

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Correspondence to V. S. Prassolov.

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Original Russian Text © N.N. Orlova, T.D. Lebedev, P.V. Spirin, V.S. Prassolov, 2016, published in Molekulyarnaya Biologiya, 2016, Vol. 50, No. 3, pp. 395–405.

These authors equally contributed to this work.

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Orlova, N.N., Lebedev, T.D., Spirin, P.V. et al. Key molecular mechanisms associated with cell malignant transformation in acute myeloid leukemia. Mol Biol 50, 344–352 (2016). https://doi.org/10.1134/S0026893316020187

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