The e13a2 BCR-ABL transcript negatively affects sustained deep molecular response and the achievement of treatment-free remission in patients with chronic myeloid leukemia who receive tyrosine kinase inhibitors

Cancer. 2019 May 15;125(10):1674-1682. doi: 10.1002/cncr.31977. Epub 2019 Feb 1.

Abstract

Background: Stopping tyrosine kinase inhibitor (TKI) treatment has become a realistic and safe objective for patients who have chronic myeloid leukemia (CML). Both a sustained deep molecular response (sDMR) and the lack of a molecular recurrence after TKI discontinuation are required to reach a durable treatment-free remission (TFR).

Methods: The potential predictive role of BCR-ABL transcripts in attaining an sDMR and a TFR was analyzed in a strictly consecutive, unselected series of 194 patients who were diagnosed and treated with TKIs at the authors' center.

Results: Of 173 fully evaluable patients, 67 (38.7%) had the e13a2 transcript, and 106 (61.3%) had the e14a2 transcript. Complete cytogenetic and major molecular remissions were not affected, whereas the achievement of both a DMR (P = .008) and an sDMR (P = .004) was favored significantly in patients who had the e14a2 transcript. After a median of 68 months, the sDMR rate was 39.6% in those with the e14a2 transcript and 19.4% in those with the e13a2 transcript. In addition to transcript type, both the early achievement of a molecular response and starting treatment with a second-generation TKI positively affected the attainment of an sDMR in multivariate analysis. The use of a second-generation TKI as frontline treatment increased the sDMR rate in both transcript types. However, in patients who had the e13a2 transcript, the probability of attaining an sDMR was 37% after 60 months and did not increase further despite continuing therapy. Among 51 of 60 patients who attained an sDMR after discontinuing TKIs, 24 experienced a molecular relapse, but all regained molecular remission after resuming TKI treatment. Again, transcript type influenced TFR maintenance (P = .005), because only 2 patients (3%) with the e13a2 transcript enjoyed a durable TFR compared with 25 (23.5%) of those with the e14a2 transcript.

Conclusions: The e13a2 transcript hinders the achievement of deep responses and the possibility of stopping TKI treatment in patients with CML.

Keywords: breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL) transcript; chronic myelogenous leukemia; deep molecular response; treatment-free remission; tyrosine kinase inhibitors.

Publication types

  • Comparative Study

MeSH terms

  • Academic Medical Centers
  • Adult
  • Aged
  • Aged, 80 and over
  • Cohort Studies
  • Disease-Free Survival
  • Dose-Response Relationship, Drug
  • Drug Administration Schedule
  • Female
  • Fusion Proteins, bcr-abl / genetics*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Imatinib Mesylate / administration & dosage*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality
  • Male
  • Middle Aged
  • Molecular Targeted Therapy / methods
  • Multivariate Analysis
  • Prognosis
  • Proportional Hazards Models
  • Protein Kinase Inhibitors / administration & dosage*
  • Real-Time Polymerase Chain Reaction / methods
  • Retrospective Studies
  • Survival Analysis

Substances

  • Protein Kinase Inhibitors
  • Imatinib Mesylate
  • Fusion Proteins, bcr-abl