Guest guest Posted December 13, 2005 Report Share Posted December 13, 2005 That last post of mine looked so jumbled that I'm sure few were able to follow it Unfortunately, it didn't come out as clean as I had written it on my computer (where I used different colours to differenciate between 's words and my own, so here goes a better, easier to read post. Once again, thank you so much for taking the time to share all of this with us. I have a few comments on this latest report: What an exciting thought! I hope it pans out to be that we can actually halt the progression of CML. Wow, the thought of it just makes me want to jump Measuring phosphorylation of CRKL sounds like it could be of such important clinical value (if they actually measured it in patients). Any idea why they aren't doing it? Was there any news on the new drug that was rumoured to be in trials (or soon to be in trials) that specifically targets the T315I mutation? When you talk about the 30% of medication that isn't taken, do you mean that people aren't consistant with taking their Gleevec (some days they take it, others they don't) or that they'll take half as much as they're supposed to? Or perhaps both? We can't always blame the patients either (unfortunately), it seems that there are still some doctors out there who aren't familliar enough with Gleevec and are still playing around with sub theraputic doses or playing the intermittent game (take it when you feel like it or don't take it if you don't feel like it etc). Also, how did they come to this conclusion? Is it from interviewing patients or by comparing written prescriptions with orders put in by the pharmacies? Sounds kinda high to me, so I wonder what criteria they used to form this conclusion. Is someone who missed one dose in 6 months considered to be non-complient or does it take a couple of doses? I just wonder how they define " poor adherence " . With much appreciation for your time and insight, Tracey Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 13, 2005 Report Share Posted December 13, 2005 Hi Tracey - Just quickly because I'm on the road. > > > Measuring phosphorylation of CRKL sounds like it could be of such > important clinical value (if they actually measured it in patients). > Any idea why they aren't doing it? I don't know why not - except that for most of us, measuring BCR/ABL by PCR is adequate for following our progress. One piece of good news I didn't get from ASH is that more sensitive and reliable PCR's are on their way. I'll write about that at another time. > > Was there any news on the new drug that was rumoured to be in trials > (or soon to be in trials) that specifically targets the T315I > mutation? A number of labs are working on this. I heard a talk just before I left by a drug company researcher(I don't have the name of the company in my head)who's working on this and seems to have a compound showing great promise: it targets BCR/ABL (which from now on I'm going to call BA, so save typing - lots of folks do this nowadays) in the active conformation, as opposed to the inactive, which IM targets (dasatinib, which I'll call DS from now on) targets both comformations); has the same activity against " wild type " (unmutated, that is) BA as do IM, DS and the BMS drug; but which specifically inhibits T315I mutated cells. They've only studied it in vitro so far, but in testing it against the human kinome (all known human kinases - a great new word, or new to me, anyway), it shows lower toxicity than these other drugs. They hometo bring it to phase I trial less than 2 years. One of the amazing things I'm learning here is how incredibly powerful and fast drug discovery technology has become. If only the machinery for bringing good new drugs to market were a bit faster! > > When you talk about the 30% of medication that isn't taken, do you > mean that people aren't consistant with taking their Gleevec (some > days they take it, others they don't) or that they'll take half as > much as they're supposed to? Or perhaps both? Both, I think. Of course, I am one of these patients, but I do my pulse regimen in a much more rigorous (and, I hope, safe) way than arbitrarily skipping doses when I feel like it. Btw, there was a lot of interest by researchers here in what I'm doing. > > Also, how did they come to this conclusion? Is it from interviewing > patients or by comparing written prescriptions with orders put in by > the pharmacies? The latter - scripts filled less frequently than expected. See ya later, R Quote Link to comment Share on other sites More sharing options...
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