Open AccessBiological Mechanisms of Sustaining Deep Molecular Response in Chronic Myeloid Leukemia Upon Withdrawal of Tyrosine Kinase Inhibitors
Author(s) -
Ekaterina Chelysheva,
Margarita Gurianova,
Anna Turkina
Publication year - 2021
Publication title -
kliničeskaâ onkogematologiâ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.116
H-Index - 2
eISSN - 2500-2139
pISSN - 1997-6933
DOI - 10.21320/2500-2139-2021-14-4-427-435
Subject(s) - myeloid leukemia , tyrosine kinase , discontinuation , tyrosine kinase inhibitor , clone (java method) , medicine , minimal residual disease , leukemia , immunology , cancer research , oncology , cd135 , biology , receptor , cancer , gene , genetics
The feasibility of treatment-free follow-up in chronic myeloid leukemia (CML) patients is an important issue in the era of tyrosine kinase inhibitors (TKI). The clinical trials of TKI withdrawal in case of a stable deep molecular response prove the probability of sustaining molecular remission in 40-60 % of patients. Treatment-free remission (TFR), even under persistence of residual leukemia cells, suggests that there are special biologically determined mechanisms of tumor cell proliferation control, which are independent of BCR-ABL kinase activity. The search for factors determining differences in residual leukemia clone kinetics upon TKI withdrawal is an objective which is crucial for understanding TFR as a new biological phenomenon. The review provides worldwide evidence dealing with the study of immunological, genetic, and other biological mechanisms underlying the control of minimal residual disease upon TKI discontinuation in CML patients.