Background
Methotrexate (MTX) remains a critical component in the treatment of
pediatric acute lymphoblastic leukemia (ALL), exerting its antileukemic
effect through interference of the folate metabolic pathway. MTHFR is an
enzyme that serves as the rate limiting step within this pathway and
there has been speculation that certain MTHFR single nucleotide
polymorphisms (SNPs) alter physiologic responses to MTX and affects drug
toxicity.