Abstract
BackgroundETS2 is a downstream effector of the RAS/RAF/ERK pathway, which plays a critical role in the development of malignant tumor. However, the clinical impact of ETS2 expression in AML remains unknown. MethodsIn this study, we evaluated the prognostic significance of ETS2 expression using two relatively large cohorts of AML patients.ResultsIn the first cohort, compared to low expression of ETS2 (ETS2low), high expression of ETS2 (ETS2high) showed significant shorter OS, EFS and RFS in the current treatments including the allogeneic HCT group (n = 72) and the chemotherapy group (n = 100). Notably, among ETS2high patients, those received allogeneic HCT had longer OS, EFS and RFS than those with chemotherapy alone (allogeneic HCT, n = 39 vs. chemotherapy, n = 47), but treatment modules play insignificant role in the survival of ETS2low patients (allogeneic HCT, n = 33 vs. chemotherapy, n = 53). Moreover, gene/microRNA expression data provides insights into the biological changes associated with varying ETS2 expression levels in AML. The prognostic value of ETS2 was further validated in the second AML cohort (n = 329).ConclusionsOur results indicate that ETS2high is a poor prognostic factor in AML and may guide treatment decisions towards allogeneic HCT.
Highlights
ETS2 is a downstream effector of the RAS/RAF/ERK pathway, which plays a critical role in the development of malignant tumor
ETS2 was initially characterized as a proto-oncogene acute megakaryocytic leukemia (AMKL) [10], the clinical impact of ETS2 expression in Acute myeloid leukemia (AML) remains unknown
Expression of ETS2 in AML patients and normal controls A microarray dataset of bone marrow (BM) samples was used for differential expression analysis, including 30 AML BM and 17 normal BM (NBM) samples (GSE37307, http://www.ncbi.nlm.nih.gov/geo), and 62 AML BM and 42 NBM samples (GSE63270, http://www.ncbi.nlm.nih. gov/geo)
Summary
ETS2 is a downstream effector of the RAS/RAF/ERK pathway, which plays a critical role in the development of malignant tumor. The clinical impact of ETS2 expression in AML remains unknown. Acute myeloid leukemia (AML) represents a group of myeloid malignancies with remarkably heterogeneous outcomes [1]. A few prognosticators have been established, including mutations in NPM1 and double CEBPA that are associated with favourable outcomes; V-ets avian erythroblastosis virus E26 oncogene homolog 2 (ETS2), a downstream target for both the Ras/ Raf/MAP kinase and phosphatidylinositol 3-kinase/Akt pathways. ERG, one of the classic prognostic markers in AML, belongs to the ETS family. ETS2 was initially characterized as a proto-oncogene acute megakaryocytic leukemia (AMKL) [10], the clinical impact of ETS2 expression in AML remains unknown
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