Hi,
I've lurked around your site for quite some time. I was Dx with CML in May 2009 with a wbc count of 321,000. I went on to Glivec / Imatinib 400mg after a few weeks on Hydroxyurea to bring the counts down a bit. That pushed me towards CCyR (I was at 2 out of 100 cells at my second follow up BM after 12 months) although my PB wbc BCR/Abl ratio was stuck at between 7% and 6% for the last 6 months or so. So the doctor has managed to get my medication changed - for which I am very grateful - to Dasatinib 100mg (commencing 16 months into treatment) as clearly my reponse to date, whilst not 'failing' (less than MCyR or 35 out of 100) is sub-optimal.
I have hopes that the Dasatinib will - because of the potency - push me past CCyR and towards MMR (or better) in a fairly short period. I'm not aware of any specific mutation status I may have at present - as my conversations with my haematologist are a bit perfunctory to be honest - and I haven't asked. (Don't want to know, really!!)
My feelings:
Obviously diagnosis with CML, at 45, was a great shock - as I hadn't really taken notice of my phyisical condition by the time I did go to my GP about 'back pain'. This was due to a massively enlarged spleen. I'd also been having quite a bit of acid reflux, weight loss (both probably due to gastric restriction) and significant breathlessness (anemia) by then.
Anyway a scary moment to say the least. Thankfully I had the loving support of my family and the assurance of the doctor that modern treatment was (mostly) effective. As I initially responded rapidly to the treatment - and general health was not so much restored as transformed in a matter of weeks, I started to find hope again. But I it took rather longer - most of that year - before that I allowed myself to feel cautiously justified in that hope. I also had a bout of mild depression (anxiety, really) in the meantime as the first BM follow approached - the results of which were disappointing.
Now that the disease appears to be under control (although not as much as would be liked) I am amazed at how my feelings have changed towards the positive. There is no reason, certainly, to assume 'the worst' at this stage. And the reasons to be hopeful seem to gain weight with time. For instance, when told that I probably needed to switch drugs I could have seen that as a 'failure' or a 'defeat'. Instead I accepted it in terms of 'aiming higher' - a 'glass half full' perspective if you please. The Sprycel - I tell myself - is designed to bind to the rogue BCR/Abl even tigher than Imatinib. Also, the theraputic dose is just 100mg - one quarter of standard Glivec - hence it must be 'good stuff' and my liver cells could do with the rest. Another boon is that Sprycel can be taken without food - and thus at any convenient fixed time (eg when out and about)
Unlike post-diagnosis - when the term 'blast crisis' kept beating around inside my head - I can take a clear interest in the disease. Sometimes I read something which makes me feel slightly vulnerable again - but mostly the information I am getting is unremittingly positive. Let me make a rather bold statement which I'm cofident is true: Whilst I may not make it through, long term, nearly all of you fellow CMLers, reading this, WILL! That's a fact which needs to imparted I feel.
TKIs (including, it appears to be case, Imatinib) largely squeeze the disease down to a pea and keep it there. There is even evidence of complete clearance of disease by Imatinib alone in a modest but significant number of cases - allowing suspension of all treatment. So, just think how second generation TKIs, if given as frontline treatment, will raise that bar? When Imatinib was discovered they didn't really how it worked as well as it did - just that it did work! Now that the mechanisms of disease progression are being studied ever closer new insights are emerging which allow better results to be achieved whatever TKI is selected - as they all work slightly differently - to shut down and 'silence' the BCR/Abl protein.
I've not seen anyone mention here yet a new drug - ponatinib (AP24534) - which has the potential to completely inhibit the dreaded T315I mutation. If they have cracked that one, BCR/Abl must surely be defeated finally? But I suspect no one will be satisfied until newer TKI's are shown to be permanently effective against advanced/blast crisis disease. (How close is that day now?)
Anyway I've gone on far too long already - but I just wanted to introduce myself
Love,
Paul
