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- W123269666 abstract "The advances in structural biology have facilitated a detailed understanding of many enzyme-substrate interactions at the molecular level. This information has been used in conjunction with techniques in site-directed and random mutagenesis to rationally generate mutant forms of drug resistance genes. Mutations in the active binding site of dihydrofolate reductase (DHFR) have been shown to markedly reduce the affinity of methotrexate (MTX) and trimetrexate (TMTX) for DHFR. Myeloprotection or bone marrow protection with these mutant forms of DHFR was originally demonstrated using the N2A-based double-copy vector containing the simian virus 40 (SV40) promoter. Transduction of the mutant DHFR cDNA into murine hematopoietic progenitor cells (mHPCs) conferred significant resistance to 100 nM MTX. These observations were extended to human hematopoietic progenitor cells (hHPC). The results demonstrated both the feasibility and efficiency of ex vivo CD34 + stem cell transduction with this retroviral vector and in vivo selection in the presence of MTX. The cytokines required for successful ex vivo expansion and transduction were subsequently refined in further studies using the same gene transfer system in HPCs from patients undergoing autologous stem cell transplantation for solid tumors." @default.
- W123269666 created "2016-06-24" @default.
- W123269666 creator A5002126535 @default.
- W123269666 date "2002-01-01" @default.
- W123269666 modified "2023-09-25" @default.
- W123269666 title "Development and Application of an Engineered Dihydrofolate Reductase and Cytidine-Deaminase-Based Fusion Genes in Myeloprotection-Based Gene Therapy Strategies" @default.
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- W123269666 doi "https://doi.org/10.1016/b978-012437551-2/50024-0" @default.
- W123269666 hasPublicationYear "2002" @default.
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