title: Achieving deeper molecular response is associated with a better clinical outcome in chronic myeloid leukemia patients on imatinib front-line therapy.
abstract: Sustained imatinib treatment in chronic myeloid leukemia patients can result in complete molecular response allowing discontinuation without relapse. We set out to evaluate the frequency of complete molecular response in imatinib de novo chronic phase chronic myeloid leukemia patients, to identify base-line and under-treatment predictive factors of complete molecular response in patients achieving complete cytogenetic response, and to assess if complete molecular response is associated with a better outcome. A random selection of patients on front-line imatinib therapy (n=266) were considered for inclusion. Complete molecular response was confirmed and defined as MR 4.5 with undetectable BCR-ABL transcript levels. Median follow up was 4.43 years (range 0.79-10.8 years). Sixty-five patients (24%) achieved complete molecular response within a median time of 32.7 months. Absence of spleen enlargement at diagnosis, achieving complete cytogenetic response before 12 months of therapy, and major molecular response during the year following complete cytogenetic response was predictive of achieving further complete molecular response. Patients who achieved complete molecular response had better event-free and failure-free survivals than those with complete cytogenetic response irrespective of major molecular response status (95.2% vs. 64.7% vs. 27.7%, P=0.00124; 98.4% vs. 82.3% vs. 56%, P=0.0335), respectively. Overall survival was identical in the 3 groups. In addition to complete cytogenetic response and major molecular response, further deeper molecular response is associated with better event-free and failure-free survivals, and complete molecular response confers the best outcome.
authors.affiliation: g.etienne@bordeaux.unicancer.fr.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Etienne
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Dulucq
authors.forename: Franck-Emmanuel
authors.initials: FE
authors.lastname: Nicolini
authors.forename: Stéphane
authors.initials: S
authors.lastname: Morisset
authors.forename: Marie-Pierre
authors.initials: MP
authors.lastname: Fort
authors.forename: Anna
authors.initials: A
authors.lastname: Schmitt
authors.forename: Madeleine
authors.initials: M
authors.lastname: Etienne
authors.forename: Sandrine
authors.initials: S
authors.lastname: Hayette
authors.forename: Eric
authors.initials: E
authors.lastname: Lippert
authors.forename: Caroline
authors.initials: C
authors.lastname: Bureau
authors.forename: Isabelle
authors.initials: I
authors.lastname: Tigaud
authors.forename: Didier
authors.initials: D
authors.lastname: Adiko
authors.forename: Gérald
authors.initials: G
authors.lastname: Marit
authors.forename: Josy
authors.initials: J
authors.lastname: Reiffers
authors.forename: François-Xavier
authors.initials: FX
authors.lastname: Mahon
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001549:Benzamides / Q000008:administration & dosage / Q000627:therapeutic use*; D002869:Chromosome Aberrations; D005260:Female; D005500:Follow-Up Studies; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality; D008297:Male; D008875:Middle Aged; D010879:Piperazines / Q000008:administration & dosage / Q000627:therapeutic use*; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D011743:Pyrimidines / Q000008:administration & dosage / Q000627:therapeutic use*; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl