Evaluation of Residual Disease and TKI Duration Are Critical Predictive Factors for Molecular Recurrence after Stopping Imatinib First-line in Chronic Phase CML Patients.
Adult
Aged
Drug Administration Schedule
Female
Fusion Proteins, bcr-abl
/ genetics
Gene Expression Regulation, Leukemic
Humans
Imatinib Mesylate
/ therapeutic use
Leukemia, Myeloid, Chronic-Phase
/ drug therapy
Male
Middle Aged
Neoplasm Recurrence, Local
Neoplasm, Residual
/ diagnosis
Prognosis
Prospective Studies
Protein Kinase Inhibitors
/ therapeutic use
Remission Induction
Survival Analysis
Treatment Outcome
Journal
Clinical cancer research : an official journal of the American Association for Cancer Research
ISSN: 1557-3265
Titre abrégé: Clin Cancer Res
Pays: United States
ID NLM: 9502500
Informations de publication
Date de publication:
15 11 2019
15 11 2019
Historique:
received:
15
10
2018
revised:
21
01
2019
accepted:
03
07
2019
pubmed:
12
7
2019
medline:
4
8
2020
entrez:
12
7
2019
Statut:
ppublish
Résumé
Tyrosine kinase inhibitor (TKI) discontinuation is an emerging goal in chronic myelogenous leukemia (CML) management and several studies have demonstrated the feasibility of safely stopping imatinib. A sustained deep molecular response on long-term TKI is critical prior to attempting treatment-free remission. Reproducible results from several studies reported recently, failed to identify robust and reproducible predictive factors for the selection of the best candidates for successful TKI cessation. We conducted a prospective national phase II study evaluating the cessation of imatinib after at least 2 years of MR4.5 obtained on imatinib first-line in patients with chronic phase CML. A total of 218 patients with We conclude that the duration of TKI and residual leukemic cell load as determined by ddPCR are key factors for predicting successful treatment-free remission for patients with
Identifiants
pubmed: 31292142
pii: 1078-0432.CCR-18-3373
doi: 10.1158/1078-0432.CCR-18-3373
doi:
Substances chimiques
Protein Kinase Inhibitors
0
Imatinib Mesylate
8A1O1M485B
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Clinical Trial, Phase II
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6606-6613Commentaires et corrections
Type : CommentIn
Informations de copyright
©2019 American Association for Cancer Research.