I am kind of on hold right now waiting for the powers that be to decide what drug will be next. I have been on Gleevec and Tasigna and my levels are rising again. I had a mutation test between the Gleevec and the Tasigna and there were no mutations. My question is why are these drugs not working? Is CML all the same except for the type with a mutation or are there different levels that are harder to deal with. Does this make any sense? I am just looking for a reason I guess. If my CML has no mutation why won't it respond?
Are there different "types" of CML.
Posted 20 April 2011 - 09:15 PM
A kinase mutation is less likely to be the cause of poor drug response than other factors. Other factors include: 1) poor cell uptake of drugs (some have better uptake than others), and sometimes increased dosage can help; 2) over-expression of LYN; I know, it is a technical issue, but this can inhibit TKI drug action. Sprycel can overcome this issue better than the others since it inhibits SRC, and LYN is a subset of SRC. It is a three-beer discussion, and I don't have three beers in me right now.... 3) other factors that are not well understood.
So rather than speculate on what might not happen, switch to Sprycel and see if it works.
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