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Phase 3 N=800 Randomized Treatment

05-001: Treatment of Acute Lymphoblastic Leukemia in Children

Drug/Agent Toxicity by Tissue/Organ · Leukemia

Enrolled (actual)
800
Serious AEs
67.5%
Results posted
Jun 2017
Primary outcome: Primary: Asparaginase-Related Toxicity Rate — 26; 28 percentage of participants — p=.60

Study Design & Population

Study type
Interventional
Phase
Phase 3
Interventions
asparaginase (Drug); cyclophosphamide (Drug); cytarabine (Drug); dexamethasone (Drug); dexrazoxane hydrochloride (Drug); doxorubicin hydrochloride (Drug); etoposide (Drug); leucovorin calcium (Drug); mercaptopurine (Drug); methotrexate (Drug); methylprednisolone (Drug); pegaspargase (Drug); prednisolone (Drug); therapeutic hydrocortisone (Drug); vincristine sulfate (Drug); radiation therapy (Radiation)
Age
Pediatric, Adult · 1+ yrs
Sex
All
Sponsor
Dana-Farber Cancer Institute
Primary completion
Aug 2014

Outcome Measures

OutcomeResultp-value
PRIMARY
Asparaginase-Related Toxicity Rate
26; 28 .60
SECONDARY
5-Year Disease-Free Survival
.89; .90
SECONDARY
Post-Induction Nadir Serum Asparaginase Activity Level
0.129; 0.726; 0.143; 0.773; 0.159; 0.787
SECONDARY
Post-Induction Therapeutic Nadir Serum Asparaginase Activity Rate
71; 99
SECONDARY
Induction Infection Toxicity Rate
26
SECONDARY
Induction Serum Asparaginase Activity Level
.694; .505; .211; .048
SECONDARY
Induction Therapeutic Nadir Serum Asparaginase Activity Rate
97; 96; 87; 12
SECONDARY
5-Year Disease-Free Survival by MRD Day 32 Status
.79; .90
SECONDARY
5-Year Disease-Free Survival by Bone Marrow Day 18 Status
.89; .78; .88
SECONDARY
5-year Disease-Free Survival by CNS Directed Treatment Group
.89; .89; 1.00; .84; .87

Summary

RATIONALE: L-asparaginase is an important component of treatment for childhood acute lymphoblastic leukemia, but is also associated with notable side-effects, including hypersensitivity, pancreatitis, and thrombosis. We have previously reported that patients with acute lymphoblastic leukemia in whom asparaginase treatment was discontinued because of intolerable side-effects had survival outcomes that were inferior to those who received all or nearly all of their intended doses. Two bacterial sources of asparaginase exist: Escherichia coli (E coli) and Erwinia chrysanthemia (Erwinia). Generally, the E coli-derived enzyme has been used as front-line therapy and the Erwinia-derived preparation has been reserved for patients who develop hypersensitivity reactions. Pegylated E coli asparaginase (PEG-asparaginase) has a longer half-life and is potentially less immunogenic than native E coli L-asparaginase, and has been used as the initial asparaginase preparation in some pediatric acute lymphoblastic leukemia treatment regimens. PURPOSE: Although the pharmacokinetics of each of these asparaginase preparations: intravenous PEG-asparaginase (IV-PEG) and intramuscular native E coli L-asparaginase (IM-EC) have been well characterized, their relative efficacy and toxicity have not been studied extensively.

Eligibility Criteria

DISEASE CHARACTERISTICS:

  • Diagnosis of acute lymphoblastic leukemia (ALL)
  • No known mature B-cell ALL, defined by the presence of any of the following:
  • Surface immunoglobulin
  • L3 morphology
  • t(8;14)(q24;q32)
  • t(8;22)
  • t(2;8)
  • T-cell surface markers and t(8;14)(q24;q11) allowed
  • No secondary ALL

PATIENT CHARACTERISTICS:

  • No known HIV positivity
  • Not pregnant or nursing
  • Fertile patients must use effective contraception

PRIOR CONCURRENT THERAPY:

  • No prior therapy except steroids of ≤ 1 week in duration and/or emergent radiation therapy to the mediastinum
  • Patients treated with steroids within the past 7 days will not receive steroid prophase during study treatment
View full record on ClinicalTrials.gov →

Data sourced from ClinicalTrials.gov (NCT00400946). Outcome figures and adverse-event rates are extracted automatically from the registry's posted results and are provided for clinician reference, not as a substitute for the primary publication.

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