The prognostic role of NKG2A expression for patients with chronic myeloid leukemia after treatment discontinuation

Abstract

This study aims to evaluate the possibility of tyrosine kinase inhibitors (TKIs) discontinuation in chronic myeloid leukemia (CML) patients who obtained sustained deep molecular response (DMR) and to explore the prognostic role of NK cells in treatment-free remission (TFR). Sixty CML patients who discontinued TKI treatment were enrolled, and we also investigated the immune profiles in 27 CML patients after TKI cessation. Of the 60 patients, the estimated TFR rate was 60.8% [95% CI: 49.5–74.8%] at 12 months. Patients who had longer TKI duration, major molecular response, and DMR maintenance time had a significantly higher TFR rate. And a higher percentage of NKG2A⁺NK cells and NKG2A⁺CD56^brightCD16⁻NK cells were independent prognostic factors of TFR in multivariate analysis. These results indicate the practicality of the cessation of TKIs and patients with stable NK cell counts accompanied by higher cytotoxicity and increased killing capacity are more inclined to get sustained treatment-free survival.

Keywords:

• Chronic myeloid leukemia (CML)
• tyrosine kinase inhibitor (TKI)
• treatment-free remission (TFR)
• natural killer (NK) cells
• NKG2A
• NKG2D

Author contributions

(I) Conception and design: All authors; (II) Administrative support: W. Liu, S. Qian; (III) Provision of study materials or patients: Q. Sun, M. Hong; (IV) Collection and assembly of data: Z. Xu, J. Yin, J. Hu; (V) Data analysis and interpretation: Z. Xu, J. Yin, J. Hu; (VI) Manuscript writing: Z. Xu; (VII) Final approval of manuscript: All authors.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data generated and analyzed during the current study are included in this article and its supplementary information files.

Additional information

Funding

This work was supported by grants from the National Natural Science Foundation of China [Nos 871700114, 81870119, 82170153].