Abstract：
:Previous studies have documented the roles of transport via the reduced folate carrier, retention via polyglutamylation, and increased levels of the target enzyme, dihydrofolate reductase in sensitivity to methotrexate. Recent studies have shown that the mitochondrial enzymes in the cellular metabolism of serine, folate, and glycine are overexpressed in a subset of human cancers and that their expression is required for tumor maintenance. In this Perspective article, we propose that the expression of mitochondrial enzymes in the metabolism of serine and glycine, in addition to those involved in folate metabolism, are determinants of the response to methotrexate. Furthermore, we show that myc activation in tumors is associated with upregulation of these enzymes. We propose that patients whose tumors show this phenotype will be sensitive to folate antagonists targeting thymidylate or purine biosynthesis.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Vazquez A,Tedeschi PM,Bertino JRdoi
10.1158/0008-5472.CAN-12-3709subject
Has Abstractpub_date
2013-01-15 00:00:00pages
478-82issue
2eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-12-3709journal_volume
73pub_type
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