206
Views
6
CrossRef citations to date
0
Altmetric
Original Articles: Clinical

High expression of INHBA is an adverse prognostic factor for de novo acute myeloid leukemia

, , , , &
Pages 114-120 | Received 21 Nov 2016, Accepted 22 Apr 2017, Published online: 24 Aug 2017
 

Abstract

Inhibin-β A (INHBA) is a ligand of the transforming growth factor β superfamily and associated with tumorigenesis and tumor progression in solid tumors. In this study, we investigated the expression levels and clinical significance of INHBA in acute myeloid leukemia (AML). The results showed that high expression of INHBA was significantly correlated with elderly age (>60 years) (p = .038), adverse cytogenetic risks (p = .034), negative NPM1 mutation (p = .016), positive FLT3 internal tandem duplications (p = .011), and low hemoglobin levels (<60 g/dL) (p = .04). Patients with high levels of INHBA had poor responses to therapies as indicated by lower complete remission rate (p = .004), higher early death rate (p = .018), and shorter relapse-free survival (p = .04) and overall survival (p = .003). Moreover, multivariate analysis showed that high expression of INHBA was an independent adverse prognostic factor for AML. Taken together, our study suggested that high expression of INHBA was an adverse prognostic factor for de novo AML.

Ethics, consent and permissions

All human materials were obtained with informed consents and approved by the Ethics Committee of the Yinzhou People’s Hospital.

Potential conflict of interest

Disclosure forms provided by the authors are available with the full text of this article online at https://doi.org/10.1080/10428194.2017.1324157.

Additional information

Funding

This work was supported by grants from Ningbo Natural Science Foundation (grant#2014A610232), the National Natural Science Foundation of China (grant # 81400098), and the K.C. Wong Magna Fund in Ningbo University.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.