You should consider switching drugs - dasatinib is a good option.
E13A2 and E14A2 are the major two of the many bcr-abl clones that TKI's are able to target. E13A2, however, has less favorable outcome when treated with Imatinib than E14A2. Switching to a different drug (nilotinib, dasatinib) will likely be more effective than imatinib in binding to the bcr-abl site of E13A2 leading to cell death (apoptosis). I suggest dasatinib because it is documented to target E13A2 better (see nature link above).
If you do switch to dasatinib, stress to your doctor starting at full dose sprycel 100 mg is not required. Consider starting at 70 or even 50 mg to transition off imatinib. You can always increase dasatinib dose if bcr-abl remains stubborn. But I have a suspicion your bcr-abl levels (both E13A2 and E14A2) will fall significantly after switching. Full dose sprycel at 100 mg is proving to be too high a starting dose and is associated with many adverse events (pleural effusion is the top one). Statistics are showing that many patients are having as good or even better response on 1/2 dose (50 mg) and it is quickly becoming the accepted standard.
Discuss with your doctor and inquire about TKI drug effectiveness against the bcr-abl clones you have. He/she should be knowledgeable on what to do.
(I had both clones at diagnosis and a few other things going on as well. I did not respond well to imatinib, but after switching to dasatnib, my E13A2 clone disappeared straight away. E14A2 took longer, but it too is now "undetected". I achieved my result while taking 20 mg dasatinib and only after reducing my starting dose of 70 mg.)
