Successful treatment-free remission in chronic myeloid leukaemia and its association with reduced immune suppressors and increased natural killer cells.
Adult
Aged
Aged, 80 and over
Antineoplastic Agents, Immunological
/ administration & dosage
Biomarkers
Female
Humans
Immunomodulation
/ drug effects
Killer Cells, Natural
/ drug effects
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ drug therapy
Leukocyte Count
Male
Middle Aged
Myeloid-Derived Suppressor Cells
/ drug effects
Prognosis
Protein Kinase Inhibitors
/ administration & dosage
Receptors, Natural Killer Cell
/ genetics
Recurrence
Remission Induction
Treatment Outcome
CML
immunobiology
treatment-free remission
Journal
British journal of haematology
ISSN: 1365-2141
Titre abrégé: Br J Haematol
Pays: England
ID NLM: 0372544
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
06
03
2020
revised:
12
04
2020
accepted:
13
04
2020
pubmed:
1
5
2020
medline:
23
3
2021
entrez:
1
5
2020
Statut:
ppublish
Résumé
There is currently no biomarker that reliably predicts treatment-free remission (TFR) in chronic myeloid leukaemia (CML). We characterised effector and suppressor immune responses at the time of tyrosine kinase inhibitor (TKI) cessation in patients from the CML8 and CML10 clinical studies. Natural killer (NK) cells with increased expression of activating NK receptors were higher in patients who achieved TFR. There was no difference in the proportion of CD4
Substances chimiques
Antineoplastic Agents, Immunological
0
Biomarkers
0
Protein Kinase Inhibitors
0
Receptors, Natural Killer Cell
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
433-441Subventions
Organisme : Royal Adelaide Hospital
ID : Contributing Haematologists Committee
Organisme : National Health and Medical Research Council
ID : APP1059165
Organisme : National Health and Medical Research Council
ID : APP1138935
Informations de copyright
© 2020 British Society for Haematology and John Wiley & Sons Ltd.
Références
Bower H, Bjorkholm M, Dickman PW, Hoglund M, Lambert PC, Andersson TM. Life expectancy of patients with chronic myeloid leukemia approaches the life expectancy of the general population. J Clin Oncol. 2016;34:2851-7.
Branford S, Fletcher L, Cross NC, Muller MC, Hochhaus A, Kim DW, et al. Desirable performance characteristics for BCR-ABL measurement on an international reporting scale to allow consistent interpretation of individual patient response and comparison of response rates between clinical trials. Blood. 2008;112:3330-8.
Hughes TP, Ross DM. Moving treatment-free remission into mainstream clinical practice in CML. Blood. 2016;128:17-23.
Mahon FX, Rea D, Guilhot J, Guilhot F, Huguet F, Nicolini F, et al. Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial. Lancet Oncol. 2010;11:1029-35.
Villemagne Sanchez LA, O'Callaghan C, Gough K, Hall K, Kashima Y, Seymour JF, et al. Patient perceptions of treatment-free remission in chronic myeloid leukemia. Leuk Lymphoma. 2018;59:406-15.
Dusetzina SB, Winn AN, Abel GA, Huskamp HA, Keating NL. Cost sharing and adherence to tyrosine kinase inhibitors for patients with chronic myeloid leukemia. J Clin Oncol. 2014;32:306-11.
Rea D, Mahon FX. How I manage relapse of chronic myeloid leukaemia after stopping tyrosine kinase inhibitor therapy. Br J Haematol. 2018;180:24-32.
Hughes A, Clarson J, Tang C, Vidovic L, White DL, Hughes TP, et al. CML patients with deep molecular responses to TKI have restored immune effectors and decreased PD-1 and immune suppressors. Blood. 2017;129:1166-76.
Hughes A, Yong ASM. Immune effector recovery in chronic myeloid leukemia and treatment-free remission. Front Immunol. 2017;8:469.
Ilander M, Hekim C, Mustjoki S. Immunology and immunotherapy of chronic myeloid leukemia. Curr Hematol Malig Rep. 2014;9:17-23.
Molldrem JJ, Lee PP, Wang C, Felio K, Kantarjian HM, Champlin RE, et al. Evidence that specific T lymphocytes may participate in the elimination of chronic myelogenous leukemia. Nat Med. 2000;6:1018-23.
Schurch C, Riether C, Amrein MA, Ochsenbein AF. Cytotoxic T cells induce proliferation of chronic myeloid leukemia stem cells by secreting interferon-gamma. J Exp Med. 2013;210:605-21.
Horowitz MM, Gale RP, Sondel PM, Goldman JM, Kersey J, Kolb HJ, et al. Graft-versus-leukemia reactions after bone marrow transplantation. Blood. 1990;75:555-62.
Ilander M, Olsson-Stromberg U, Schlums H, Guilhot J, Bruck O, Lahteenmaki H, et al. Increased proportion of mature NK cells is associated with successful imatinib discontinuation in chronic myeloid leukemia. Leukemia. 2017;31:1108-16.
Imagawa J, Tanaka H, Okada M, Nakamae H, Hino M, Murai K, et al.; Group, D.T. Discontinuation of dasatinib in patients with chronic myeloid leukaemia who have maintained deep molecular response for longer than 1 year (DADI trial): a multicentre phase 2 trial. Lancet Haematol. 2015;2:e528-535.
Ohyashiki K, Katagiri S, Tauchi T, Ohyashiki JH, Maeda Y, Matsumura I, et al. Increased natural killer cells and decreased CD3(+)CD8(+)CD62L(+) T cells in CML patients who sustained complete molecular remission after discontinuation of imatinib. Br J Haematol. 2012;157:254-6.
Rea D, Henry G, Khaznadar Z, Etienne G, Guilhot F, Nicolini F, et al. Natural killer-cell counts are associated with molecular relapse-free survival after imatinib discontinuation in chronic myeloid leukemia: the IMMUNOSTIM study. Haematologica. 2017;102:1368-77.
Ross DM, Branford S, Seymour JF, Schwarer AP, Arthur C, Yeung DT, et al. Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER study. Blood. 2013;122:515-22.
Kotsakis A, Harasymczuk M, Schilling B, Georgoulias V, Argiris A, Whiteside TL. Myeloid-derived suppressor cell measurements in fresh and cryopreserved blood samples. J Immunol Methods. 2012;381:14-22.
Tompa A, Nilsson-Bowers A, Faresjö M. Subsets of CD4(+), CD8(+), and CD25(hi) lymphocytes are in general not influenced by isolation and long-term cryopreservation. J Immunol. 2018;201:1799-809.
Friedman J, Hastie T, Tibshirani R. Regularization paths for generalized linear models via coordinate descent. J Stat Softw. 2010;33:1-22.
Oehler VG, Yeung KY, Choi YE, Bumgarner RE, Raftery AE, Radich JP. The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data. Blood. 2009;114:3292-8.
Kuhn M. Building Predictive Models inRUsing thecaretPackage. J Stat Softw. 2008;28:26.
Ross DM, Pagani IS, Shanmuganathan N, Kok CH, Seymour JF, Mills AK, et al. Long-term treatment-free remission of chronic myeloid leukemia with falling levels of residual leukemic cells. Leukemia. 2018;32:2572-9.
Aldemir H, Prod'homme V, Dumaurier MJ, Retiere C, Poupon G, Cazareth J, et al. Cutting edge: lectin-like transcript 1 is a ligand for the CD161 receptor. J Immunol. 2005;175:7791-5.
Schlums H, Cichocki F, Tesi B, Theorell J, Beziat V, Holmes TD, et al. Cytomegalovirus infection drives adaptive epigenetic diversification of NK cells with altered signaling and effector function. Immunity. 2015;42:443-56.
Saussele S, Richter J, Guilhot J, Gruber FX, Hjorth-Hansen H, Almeida A, et al. Discontinuation of tyrosine kinase inhibitor therapy in chronic myeloid leukaemia (EURO-SKI): a prespecified interim analysis of a prospective, multicentre, non-randomised, trial. Lancet Oncol. 2018;19:747-57.
Lanier LL, Corliss B, Wu J, Phillips JH. Association of DAP12 with activating CD94/NKG2C NK cell receptors. Immunity. 1998;8:693-701.
Rolle A, Meyer M, Calderazzo S, Jager D, Momburg F. Distinct HLA-E peptide complexes modify antibody-driven effector functions of adaptive NK cells. Cell Rep. 2018;24(1967-1976):e1964.
Koch J, Steinle A, Watzl C, Mandelboim O. Activating natural cytotoxicity receptors of natural killer cells in cancer and infection. Trends Immunol. 2013;34:182-91.
Ross DM, Pagani IS, Irani YD, Clarson J, Leclercq T, Dang P, et al. Lenalidomide maintenance treatment after imatinib discontinuation: results of a phase 1 clinical trial in chronic myeloid leukaemia. Br J Haematol. 2019;186:e56-e60.
Schutz C, Inselmann S, Saussele S, Dietz CT, Mu Ller MC, Eigendorff E, et al. Expression of the CTLA-4 ligand CD86 on plasmacytoid dendritic cells (pDC) predicts risk of disease recurrence after treatment discontinuation in CML. Leukemia. 2017;31:829-36.
Claudiani S, Apperley JF, Gale RP, Clark R, Szydlo R, Deplano S, et al. E14a2 BCR-ABL1 transcript is associated with a higher rate of treatment-free remission in individuals with chronic myeloid leukemia after stopping tyrosine kinase inhibitor therapy. Haematologica. 2017;102:e297-e299.
Fontenot JD, Gavin MA, Rudensky AY. Foxp3 programs the development and function of CD4+CD25+ regulatory T cells. Nat Immunol. 2003;4:330-6.
Okada M, Imagawa J, Tanaka H, Nakamae H, Hino M, Murai K, et al, Dadi Trial Group, J. Final 3-year results of the dasatinib discontinuation trial in patients with chronic myeloid leukemia who received dasatinib as a second-line treatment. Clin Lymphoma Myeloma Leuk. 2018;18(353-360):e351.
Gabrilovich DI, Ostrand-Rosenberg S, Bronte V. Coordinated regulation of myeloid cells by tumours. Nat Rev Immunol. 2012;12:253-68.
Giallongo C, Parrinello NL, La Cava P, Camiolo G, Romano A, Scalia M, et al. Monocytic myeloid-derived suppressor cells as prognostic factor in chronic myeloid leukaemia patients treated with dasatinib. J Cell Mol Med. 2018;22:1070-80.