Figure 4.
Figure 4. Fludarabine enhances the oxaliplatin-induced DNA interstrand crosslinks in the DHFR gene in normal or CLL lymphocytes. DNA from CLL lymphocytes incubated in absence or presence of fludarabine for 2 hours before exposure to increasing concentrations of oxaliplatin for 7 hours was isolated and analyzed for ICL formation. (A) Representation of HindIII-digested DNA denatured and electrophoresed through a 0.5% agarose gel, before being transferred to nylon and probed for a 22-kb DHFR gene fragment. DS indicates double-strand DNA; SS, single-strand DNA. The data shown were based on at least 3 independent experiments, and DNA samples from each biologic experiment were subjected to gel electrophoresis and Southern analysis at least twice. Crosslinks in the DHFR gene in normal lymphocytes (B) or CLL lymphocytes (C); this value was normalized to ICL/10 kb in the absence (▪) or presence (•) of 2.5 μM fludarabine, expressed as the mean ± SE (n = 3).

Fludarabine enhances the oxaliplatin-induced DNA interstrand crosslinks in the DHFR gene in normal or CLL lymphocytes. DNA from CLL lymphocytes incubated in absence or presence of fludarabine for 2 hours before exposure to increasing concentrations of oxaliplatin for 7 hours was isolated and analyzed for ICL formation. (A) Representation of HindIII-digested DNA denatured and electrophoresed through a 0.5% agarose gel, before being transferred to nylon and probed for a 22-kb DHFR gene fragment. DS indicates double-strand DNA; SS, single-strand DNA. The data shown were based on at least 3 independent experiments, and DNA samples from each biologic experiment were subjected to gel electrophoresis and Southern analysis at least twice. Crosslinks in the DHFR gene in normal lymphocytes (B) or CLL lymphocytes (C); this value was normalized to ICL/10 kb in the absence (▪) or presence (•) of 2.5 μM fludarabine, expressed as the mean ± SE (n = 3).

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