Could this variability be related to the efficacy and integrity of their DNA repair pathway and/ or the strength of their ABC transporter system? Other factors maybe? I can understand that this is a very simplistic way to the issue, but any input on the subject will help many to know what are those factors that modulate the efficacy of 5-Aza on different target cell lines
I am wondering whether differences in the rate of cell replication can account for the differences in dose and duration of treatment to realize the effects of 5-Azacytidine in various cell lines.
Thanks! Of course I think that should be the main factor when considering the efficiency and the integrity of all other pathways (DNA repair, DNA replication checkpoint) similar among cell lines. Because 5-deoxyAza traps covalently DNMTs to the DNA, cell needs to remove the DNA/DNMTs adduct by cutting and then repairing.
Also, what about the ABC cassette? Cell may just pump out whatever drug one put in. For example some cancer cell lines obtained from patients which have been hard-hit with drug-treatment may have their ABC cassette very active.
That may partly explain the modest benefit of treating cancer patients with decitabine.
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