Back to Search Start Over

Overexpression ofmiR-216b: Prognostic and predictive value in acute myeloid leukemia

Authors :
Jun Qian
Ting-Juan Zhang
Jiang Lin
Jing-Dong Zhou
Xi-xi Li
Ji-chun Ma
Zhao-Qun Deng
De-Hong Wu
Hong Guo
Wei Zhang
Source :
Journal of Cellular Physiology. 233:3274-3281
Publication Year :
2017
Publisher :
Wiley, 2017.

Abstract

Accumulating studies have shown that miR-216b acted as a tumor suppressor and was down-regulated in solid tumors. However, little studies revealed the role or clinical implication of miR-216b in blood cancers. Herein, we reported miR-216b expression and its clinical significance in patients with acute myeloid leukemia (AML). In the current study, we analyzed bone marrow (BM) miR-216b expression in 115 de novo AML patients examined by real-time quantitative PCR. Notably, BM miR-216b expression was significantly up-regulated in AML patients, and could serve as a potential biomarker distinguishing AML from controls. No significant correlations of BM miR-216 expression were found with sex, age, white blood cells, hemoglobin, platelets, BM blasts, French-American-British classifications, and karyotypes. Significantly, patients with high miR-216b expression tended to have a lower frequency of FLT3-ITD mutation and higher incidence of U2AF1 and IDH1/2 mutations. Moreover, complete remission (CR) rate and overall survival were negatively affected by BM miR-216b overexpression among cytogenetically normal AML (CN-AML). Cox regression analyses showed that high BM miR-216b expression may act as an independent risk factor in CN-AML patients. Among the follow-up patients, BM miR-216b level in CR phase was markedly lower than in diagnosis time, and was returned in relapse phase. Collectively, our findings indicated that miR-216b overexpression was a frequent event in de novo AML, and independently conferred a poor prognosis in CN-AML. Moreover, miR-216b expression was a valuable biomarker correlated with disease recurrence in AML.

Details

ISSN :
00219541
Volume :
233
Database :
OpenAIRE
Journal :
Journal of Cellular Physiology
Accession number :
edsair.doi.dedup.....923b62387b27cf72c909b324fe8c6406
Full Text :
https://doi.org/10.1002/jcp.26171