Cancer medicine · 2019
Killer immunoglobulin-like receptor genotypes and chronic myeloid leukemia outcomes after imatinib cessation for treatment-free remission.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Dumas Pierre-Yves, Bérard Emilie, Bréal Claire, Dulucq Stéphanie, Réa Delphine, Nicolini Franck, Forcade Edouard, Dufossée Melody, Pasquet Jean-Max, Turcq Béatrice, Bidet Audrey, Milpied Noel, Déchanet-Merville Julie, Lafarge Xavier, Etienne Gabriel, Mahon François-Xavier, French Intergroup in Chronic Myeloid Leukemia
Аннотация
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.
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.
Предметные рубрики MeSH
AgedAntineoplastic AgentsBiomarkersFemaleGenetic VariationGenotypeHaplotypesHumansImatinib MesylateImmunophenotypingKiller Cells, NaturalLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedProtein Kinase InhibitorsReceptors, KIRReceptors, KIR2DL5Remission InductionTreatment OutcomeWithholding Treatment