Publication Date:
2019-11-13
Description:
Background: After long-term treatment with tyrosine kinase inhibitors (TKIs), an important proportion of patients with chronic myeloid leukemia (CML) achieve and maintain a deep molecular response (DMR) that allows them to stop treatment indefinitely. However, approximately 50% of these patients on treatment-free remission (TFR) experience relapse by undetermined reasons. It has been described that TKIs may induce a potent antileukemic response that conditions the outcome of the discontinuation. Our objective was to analyze different immune parameters that could be used as biomarkers of safer treatment discontinuation. Objectives: To determine the modulation of immune biomarkers that could be related to current treatment with TKIs on patients with CML ("On TKI") or to successful TFR in patients that maintain DMR after treatment withdrawal ("Off TKI") or to relapse after TFR on patients that lost DMR. Materials & methods: We analyzed by flow cytometry the peripheral blood mononuclear cells (PBMCs) from 45 patients with CML "On TKI" for at least 9 months (imatinib (11), nilotinib (9), dasatinib (20) or bosutinib (5)), 17 patients "Off TKI" for at least 7 months who kept DMR at the moment of sampling (last TKI before TFR: imatinib (7), nilotinib (6), dasatinib(4)), 7 patients "Off TKI" for at least 1 year and 4 months who relapsed during TFR (samples from 3 patients were taken previous to TKI reintroduction (on relapse); samples from 4 patients were taken after they restarted treatment with TKIs ("On TKI" relapse), 4 patients with recent diagnosis of CML still untreated, and 20 healthy donors as basal control. Results: 1) Patients characteristics are shown in table 1. 2) Treatment with TKIs induced an increase of 8.6±1.2% ((p4%; CD86+
Print ISSN:
0006-4971
Electronic ISSN:
1528-0020
Topics:
Biology
,
Medicine
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