Effects of methylenetetrahydrofolate reductase and reduced folate carrier 1 polymorphisms on high-dose methotrexate-induced toxicities in children with acute lymphoblastic leukemia or lymphoma

J Pediatr Hematol Oncol. 2006 Feb;28(2):64-8. doi: 10.1097/01.mph.0000198269.61948.90.

Abstract

The authors investigated whether high-dose methotrexate-induced toxicity differed according to the presence of methylenetetrahydrofolate reductase (MTHFR) or reduced folate carrier 1 (RFC1) genetic polymorphism. The authors studied 15 children with acute lymphoblastic leukemia or lymphoblastic lymphoma who were treated using protocols that included high-dose methotrexate (3.0 g/m), for an overall total of 43 courses. Methotrexate-induced toxicities and the plasma methotrexate concentrations were evaluated retrospectively. Hematologic toxicity was the most frequently observed toxicity, appearing in 87% of the patients. In a subset of patients (47%), elevation of liver transaminase levels showed a repeated tendency to develop. High plasma methotrexate concentrations at 48 hours after the methotrexate infusion were not significantly related to methotrexate-induced toxicities except for mucositis. A generalized estimating equation analysis revealed that vomiting during the high-dose methotrexate treatment was more pronounced in patients who had a larger number of G alleles at the RFC1 80G>A polymorphism. No significant differences in the development of other toxicities or in the plasma methotrexate concentrations were observed for the different MTHFR 677C>T or RFC1 80G>A polymorphisms. This study suggests but does not prove that the RFC1 80G>A polymorphism may contribute to interindividual variability in responses to high-dose methotrexate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Alleles
  • Antimetabolites, Antineoplastic / administration & dosage
  • Antimetabolites, Antineoplastic / adverse effects*
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Chemical and Drug Induced Liver Injury / etiology*
  • Chemical and Drug Induced Liver Injury / genetics
  • Child
  • Child, Preschool
  • Female
  • Genetic Predisposition to Disease
  • Genetic Variation
  • Hematologic Diseases / chemically induced*
  • Hematologic Diseases / genetics
  • Humans
  • Infant
  • Japan
  • Male
  • Methotrexate / administration & dosage
  • Methotrexate / toxicity*
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • Polymorphism, Genetic*
  • Polymorphism, Single Nucleotide
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy*
  • Retrospective Studies
  • Stomatitis / chemically induced

Substances

  • Antimetabolites, Antineoplastic
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • Methotrexate