ArticleGene therapy2000
Selection of HSV-1 TK gene-transfected murine mammary carcinoma cells resistant to (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) and ganciclovir (GCV).
Article in Gene therapy, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 7 citations in OpenAlex.
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We evaluated the molecular mechanism of resistance in herpes simplex virus type 1 (HSV-1) thymidine kinase (TK) gene-transfected murine mammary carcinoma (FM3ATK-/HSV-1 TK+) cells, that were selected for resistance against (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) and ganciclovir (GCV) by prolonged exposure of the cell cultures to dose-escalating concentrations of these compounds. Drug-resistant FM3ATK-/HSV-1 TK+ cells showed marked differences in their sensitivity spectrum to a series of antiherpetic nucleoside analogues. BVDU-resistant FM3ATK-/HSV-1 TK+ cells displayed the same sensitivity profile as wild-type FM3A/0 cells. In contrast, GCV-resistant FM3ATK-/HSV-1 TK+ cells were still sensitive to BVDU, (E)5-(2-iodovinyl)-2'-deoxyuridine (IVDU) and (E)-5-(2bromovinyl)-2'-deoxycytidine (BVDC), a typical feature of FM3A TK cells lacking cytosolic TK. Southern blot and PCR analysis revealed that HSV-1 TK genes were not deleted from the genome of the drug-resistant FM3ATK-/HSV-1 TK+ cells. However, the TK genes in drug-resistant FM3ATK-/HSV-1 TK+ cells were shown to be heavily methylated. Accordingly, RT-PCR demonstrated the complete abrogation of TK mRNA production resulting in a complete loss of TK enzyme activity in drug-resistant FM3A TK-/HSV-1 TK+ cells.
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