Open AccessKiller immunoglobulin‐like receptor genotypes and chronic myeloid leukemia outcomes after imatinib cessation for treatment‐free remission
Author(s) -
Dumas PierreYves,
Bérard Emilie,
Bréal Claire,
Dulucq Stéphanie,
Réa Delphine,
Nicolini Franck,
Forcade Edouard,
Dufossée Melody,
Pasquet JeanMax,
Turcq Béatrice,
Bidet Audrey,
Milpied Noel,
DéchanetMerville Julie,
Lafarge Xavier,
Etienne Gabriel,
Mahon FrançoisXavier
Publication year - 2019
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.2371
Subject(s) - myeloid leukemia , imatinib , discontinuation , medicine , immunology , receptor , antibody , tyrosine kinase , minimal residual disease , leukemia , oncology , cancer research
Abstract Background Natural Killer (NK) cells are innate lymphoid cells that can be cytotoxic toward a large panel of solid tumors and hematological malignancies including chronic myeloid leukemia (CML). Such a cytotoxicity depends on various receptors. Killer immunoglobulin‐like receptors (KIR) belong to these receptors and are involved in maturation process, then in the activation abilities of NK cells. Methods: We investigated the prognostic impact of the KIR2DL5B genotype in 240 CML patients included in two clinical trials investigating tyrosine kinase inhibitors (TKI) discontinuation: STIM and STIM2. Results: After adjustment for standard risk factors in CML, we found that the inhibitory receptor KIR2DL5B‐ positive genotype was independently related to a delayed second deep molecular remission (HR 0.54, 95% CI [0.32‐0.91], P = 0.02) after TKI rechallenge but not to time to first deep molecular remission or treatment‐free remission rates. Conclusion: These results suggest that KIR2DL5B could carry a role in lymphocyte‐mediated control of leukemic residual disease control in patient with CML relapse.