Figure 5.
Figure 5. Fludarabine retards the removal of oxaliplatin-induced DNA interstrand crosslinks in the DHFR gene in normal or CLL lymphocytes. Normal lymphocytes (A) or CLL lymphocytes (B) were incubated with 400 μM oxaliplatin in the absence or presence of 2.5 μM fludarabine for 5 hours, when cells were washed into drug-free medium. DNA from cells allowed to repair for up to 8 hours was analyzed for ICL remaining in the 22-kb DHFR gene fragment. (A) Representative ICL blot probed for the DHFR gene in peripheral-blood mononuclear cells (PBMCs). The plots represent a quantitation of oxaliplatin ICLs remaining in the DHFR gene of PBMCs (B) or CLL lymphocytes (C) as a function of repair time. Crosslinks remaining after repair in the absence (▪) or presence (•) of fludarabine were expressed as a percentage of initial ICL levels.

Fludarabine retards the removal of oxaliplatin-induced DNA interstrand crosslinks in the DHFR gene in normal or CLL lymphocytes. Normal lymphocytes (A) or CLL lymphocytes (B) were incubated with 400 μM oxaliplatin in the absence or presence of 2.5 μM fludarabine for 5 hours, when cells were washed into drug-free medium. DNA from cells allowed to repair for up to 8 hours was analyzed for ICL remaining in the 22-kb DHFR gene fragment. (A) Representative ICL blot probed for the DHFR gene in peripheral-blood mononuclear cells (PBMCs). The plots represent a quantitation of oxaliplatin ICLs remaining in the DHFR gene of PBMCs (B) or CLL lymphocytes (C) as a function of repair time. Crosslinks remaining after repair in the absence (▪) or presence (•) of fludarabine were expressed as a percentage of initial ICL levels.

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