Late molecular recurrences in patients with chronic myeloid leukemia experiencing treatment-free remission.


Journal

Blood advances
ISSN: 2473-9537
Titre abrégé: Blood Adv
Pays: United States
ID NLM: 101698425

Informations de publication

Date de publication:
14 07 2020
Historique:
received: 28 02 2020
accepted: 11 05 2020
entrez: 3 7 2020
pubmed: 3 7 2020
medline: 20 5 2021
Statut: ppublish

Résumé

Treatment-free remission (TFR) is an opportunity for patients with chronic myeloid leukemia (CML). Reported cumulative incidence curves of molecular recurrence (MRec) arbor a 2-phase shape with mainly early events, but also some late events (late MRec [LMRec]). Having discontinued our first patient in 2004, we have access to a prolonged follow-up, enabling us to characterize these late events. Over 15 years, 128 patients from our institution were registered in the Stop Imatinib (STIM; A Study for Tyrosine Kinase Inhibitors Discontinuation [A-STIM]) trial. MRec was defined by the loss of major molecular response (BCR-ABL1IS >0.1%). At the first TFR attempt, patients had been taking a tyrosine kinase inhibitor for a median of 7.1 years and in BCR-ABL1IS ≤0.01% (MR4) for a median of 4 years. The median follow-up of patients in TFR was 6.5 years. The TFR rate was estimated to be 45.6% after 7 years. For 9/65 (14%) patients experiencing MRec, recurrence occurred after 2 years in TFR (median, 3.6 years). The residual rate of MRec after 2 years was estimated to be 18%. The probability of remaining in TFR was 65.4% for patients having experienced fluctuations of their minimal residual disease (MRD) (at least 2 consecutive measurements BCR-ABL1IS >0.0032% or loss of MR4), whereas it was 100% for those with stable MRD (P = .003). After 2 years in TFR, we observed an 18% residual rate of LMRec. These late events represent 14% of all MRec and occur in patients with fluctuating MRD measurements. A long-term molecular follow-up therefore remains mandatory for CML patients in TFR. The A-STIM study was registered at www.clinicaltrials.gov as #NCT02897245.

Identifiants

pubmed: 32614963
pii: S2473-9529(20)31632-3
doi: 10.1182/bloodadvances.2020001772
pmc: PMC7362352
doi:

Substances chimiques

Protein Kinase Inhibitors 0
Imatinib Mesylate 8A1O1M485B

Banques de données

ClinicalTrials.gov
['NCT02897245']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3034-3040

Informations de copyright

© 2020 by The American Society of Hematology.

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Auteurs

Philippe Rousselot (P)

Department of Hematology and Oncology, Centre Hospitalier de Versailles, Le Chesnay, France.
Unité Mixte de Recherche (UMR) 1184, Institut de Biologie François Jacob, Commissariat à lÉnergie Atomique (CEA), University of Versailles-Saint-Quentin-en-Yvelines and Paris-Saclay, France.

Clémence Loiseau (C)

Department of Hematology and Oncology, Centre Hospitalier de Versailles, Le Chesnay, France.
Unité Mixte de Recherche (UMR) 1184, Institut de Biologie François Jacob, Commissariat à lÉnergie Atomique (CEA), University of Versailles-Saint-Quentin-en-Yvelines and Paris-Saclay, France.

Marc Delord (M)

Clinical Research Center, Centre Hospitalier de Versailles, Le Chesnay, France.

Jean Michel Cayuela (JM)

Department of Molecular Biology and EA3518, University Hospital Saint-Louis Assistance Publique-Hôpitaux de Paris (AP-HP), University of Paris, Paris, France; and.

Marc Spentchian (M)

Department of Molecular Biology, Centre Hospitalier de Versailles, Le Chesnay, France.

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