3 replies to this topic

[Megz]

Hi All,

My onc gave me my BCR-ABL quant results and I need help deciphering what they means. So background info. Im in the chronic phase of CML, diagnosed in Sept 2011, started on 150mg Tasigna PO BID, then due to unresolved problems he switched me to 400mg Gleevec PO SID in June 2012. A week later he called to find out how I was doing with the new meds and to tell me that he would have switched them anyways based on my BRC-ABL results. So he said my Ph+ chromosomes are lower but that my B3A2 count was at 100% and my B2A2 is at 0%, and that no reduction in the B3A2 has occured since I started treatment (In September it was 100% too). I have no blasts which is good, and my CBC has been normal the past 6 months, although at this last appointment, everything was high normal. So the Tasigna worked on my hematological state, but not cytogenic. Anyways, he said i'm still in chronic phase because there is no basts, but what does the 100% B3A2 mean? Originally I thought if this count was higher than 10% I would have progressed further in my CML. Also, how or what decides the percentage? such as, do they look at 100 cells' chromosonal layer and if all are mutated its 100% or what, I'm pretty confused on this one thing. Plus, he keeps saying if and when the gleevec doesn't work there's some new drug he can get in Canada, which is making me freak out more, I really want the Gleevec to work.

Thanks for the help!

Meg

[CallMeLucky]

Someone like Trey can probably answer this more clearly, but basically when chromosome 9 and 22 breakoff and attach to each other to form the Philadelphia chromosome, they determine through testing where the break happened.  So B2A2 and B3A2 are breakpoints and they are the two most common.  In general Gleevec works on both of them for many people.  In most cases you would expect Tasign to work better than Gleevec.  Tasigna is a second generation TKI based on Gleevec (both made by Novartis).  That's not to say that Gleevec won't work, it is possible Tasigna would have worked against the B3A2 at some point if you had continued to take it. So Gleevec could work.  Why did you stop taking Tasigna?  It would help if you could post your results to better interpret them.  With regard to the 100% it depends if your lab is using international standard.  Assuming they are then the 100% is a an average for people diagnosed with CML in Chronic phase, think of it as the average baseline that they measure your results against.  The idea with PCR is you want to see steady declining trend.  That is why it would help to see all your results.  If your B3A2 has not budged after 10 months of treatment, that could mean something or it could not.  How long did you actually take Tasigna?  Were you off it more than on it?  You have only been on Gleevec a short time so more needs to be understood.  If the B3A2 doesn't move then a mutation test would be prudent to see if you have any mutations.  If you happen to have one that does not respond well to Tasigna, then that could explain some things.  I don't know what your doctor is talking about with going to Canada for drugs, that makes me nervous and wonder about your doctor.  I would have expected your doctor to say that the next course of treatent would be Sprycel, which is an approved TKI drug for first line treatment right here in the United States.

If I were you this is what I would do.  If you were off Tasigna more than on it, I would give the Gleevec a chance and see if it starts to work, maybe go back for another PCR 6 weeks and see how it looks.  If no improvement, then get a mutation test done and consider getting a second opinion from a CML expert.  If  you were on the Tasigna consistently, then I would probably want to get the mutation testing done sooner to see what is going on.  If you have a mutation that Gleevec doesn't help then you are wasting time.  Not that you should feel like you have an imminent issue.  CML is slow moving but at the same time if you need Sprycel, then there is no point in waiting.

[Trey]

Meg,

B3A2 and B2A2 are the two most commons forms of the Philadelphia Chromosome.  Most people have one or the other.  Your Onc seems to want to discuss both, so maybe you have both forms (so do I).  Your B2A2 is zero, and maybe it was positive at one point, so the B2A2 may have responded to drug therapy, but the B3A2 is not responding.  Ask the Onc to clarify the B2A2/B3A2 issue. 

So your B3A2 is still at 100% which is very high for having been on TKI drugs for 9 months.  This  shows that you do not appear to be responding well enough to the drug therapy.  The Tasigna low dose did not do the job, and neither did Gleevec.  A switch to Sprycel would appear to be a good idea at this point.  I don't know what the Onc meant by "some new drug he can get in Canada", but that sounds very odd, so ask about that.  I realise you have the Incontinentia Pigmenti issue you previously discussed which gets in the way somewhat, but you need to do something different. 

You should also ask the Onc to do a Kinase Mutation Test to see if you have a mutation that is preventing the drugs from working.  If so, there is one mutation that requires a different drug (Ponatinib) that is only available by clinical trial or "compassionate use" since it is not yet approved by the FDA.  But a switch now to Sprycel would be a good idea.

Hope all goes better for you. 

[Megz]

I was on Tasigna from September 15 to June 10th twice a day, I only missed lets say about two weeks of the medication due to getting sick and some "crap I forgot to take it" nights. But I took it the whole time. The gleevec i've only been on for a month and a half. I not only have CML but I have incontienta pigmenti too, as far as my onc knows, i'm the only diagnosed case in the world with both. He did say at my next apptment if the b3a2 hasn't changed he is doing the genetic test to see of i have the TKI resistance mutation. I say canada because I can't remember the name of the drug he said but he said it wasn't FDA approved yet and he could get it in Canada. My onc is Dr. Steensma at Dana Farber in boston, as far as I know he is pretty well known for CML treatment around here.