Improving the identification of high risk precursor B acute lymphoblastic leukemia patients with earlier quantification of minimal residual disease

PLoS One. 2013 Oct 11;8(10):e76455. doi: 10.1371/journal.pone.0076455. eCollection 2013.

Abstract

The stratification of patients with acute lymphoblastic leukemia (ALL) into treatment risk groups based on quantification of minimal residual disease (MRD) after induction therapy is now well accepted but the relapse rate of about 20% in intermediate risk patients remains a challenge. The purpose of this study was to further improve stratification by MRD measurement at an earlier stage. MRD was measured in stored day 15 bone marrow samples for pediatric patients enrolled on ANZCHOG ALL8 using Real-time Quantitative PCR to detect immunoglobulin and T-cell receptor gene rearrangements with the same assays used at day 33 and day 79 in the original MRD stratification. MRD levels in bone marrow at day 15 and 33 were highly predictive of outcome in 223 precursor B-ALL patients (log rank Mantel-Cox tests both P<0.001) and identified patients with poor, intermediate and very good outcomes. The combined use of MRD at day 15 (≥ 1 × 10(-2)) and day 33 (≥ 5 × 1(-5)) identified a subgroup of medium risk precursor B-ALL patients as poor MRD responders with 5 year relapse-free survival of 55% compared to 84% for other medium risk patients (log rank Mantel-Cox test, P = 0.0005). Risk stratification of precursor B-ALL but not T-ALL could be improved by using MRD measurement at day 15 and day 33 instead of day 33 and day 79 in similar BFM-based protocols for children with this disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Child
  • Cohort Studies
  • Female
  • Humans
  • Male
  • Neoplasm, Residual / diagnosis*
  • Neoplasm, Residual / pathology
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • Prognosis
  • Recurrence
  • Risk Factors

Grants and funding

This study was funded by project grants 209599 and 350886 from the National Health and Medical Research Council www.nhmrc.gov.au; a 2006 program grant from The Cancer Council NSW www.cancercouncil.com.au and a 2004 grant-in-aid from the Leukaemia Foundation www.leukaemia.org.au/. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.