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Review
. 2016 Sep 10;9(1):85.
doi: 10.1186/s13045-016-0315-9.

Aberrant splicing and drug resistance in AML

Affiliations
Review

Aberrant splicing and drug resistance in AML

Rosalia de Necochea-Campion et al. J Hematol Oncol. .

Abstract

The advent of next-generation sequencing technologies has unveiled a new window into the heterogeneity of acute myeloid leukemia (AML). In particular, recurrent mutations in spliceosome machinery and genome-wide aberrant splicing events have been recognized as a prominent component of this disease. This review will focus on how these factors influence drug resistance through altered splicing of tumor suppressor and oncogenes and dysregulation of the apoptotic signaling network. A better understanding of these factors in disease progression is necessary to design appropriate therapeutic strategies recognizing specific alternatively spliced or mutated oncogenic targets.

Keywords: Chemoresistance; Clonal evolution; Mutation; Splice factor; Target.

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Figures

Fig. 1
Fig. 1
Schematic diagram of factors influencing aberrant splicing and drug resistance in AML. TF transcription factor, SF splice factor

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