期刊
JOURNAL OF HEMATOLOGY & ONCOLOGY
卷 9, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s13045-016-0315-9
关键词
Splice factor; Chemoresistance; Mutation; Target; Clonal evolution
资金
- Loma Linda University School of Medicine, Division of Medical Oncology/Hematology Internal Research Fund
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.
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