it is difficult to make a definitive conclusion based on the information you provided. what's the leukocyte diff and bone marrow diff? if the patient had a WBC of 40K, most of them were left-shifted granulocytes (+baso,+eo) and blasts were just few. then it is CML-BP. High PLT count is uncommon in de novo AML unless it has inv(3) or t(1;22).....hepatosplenomegaly can be seen in both de novo Ph+ AL and CML-BP. Sometime after blasts are cleared up but significant number of metaphases/interphases are positive for Ph by karyotyping/FISH, retrospectively, it is CML-BP.

As Jerry said, at this point it does not matter if this was a de novo or a blast crisis. I concur completely with the transplant and if our usual thinking is correct, GVH, especially chronic GVH carries an strong element of GVL in myeloid malignancies. Normally when using a TKI post BMT, start dates are around 60 days. You do not comment on whether the GVH is being treated or not. My feeling would be that if not severe, allow to flare for a period of time. TKIs do interact with some of the GVH meds such as steroid and there is a potential issue there. Also TKIs may have anti-GVH effects. Dasatinib was originally developed as an immunosuppressant and imatinib has been studied in chronic GVHD. Personally, I would settle down the GVH after a flare, and initiate the TKI when the patient is nearly off immunosuppression. How long to continue is an undefined concept, but most of us would treat for a minimum of 2 years. Normally I choose the TKI that was used to get the patient to the allograft and have found imatinib, dasatinib and ponatinib safe in these situations. You may find that the patient does not tolerate a full dose of the TKI.

thank you for your comments. At this time I can not exclude a lab switch however I don´t think there was a switch in the lab because on July 7, 2015 at 2 different labs he had WBC of 9.3 and 9.9 with normal Hb and Platelets which is consistente with the results he had on July 20.
he has now developed aGVHD with skin and upper GIT involvement, does this contrandicate TKI?

This is a very interesting case. There is some debate whether or not de novo acute myeloid leukemia exists, but if the blood counts really were normal a mere 3 weeks before the presentation WBC of nearly 40K, then it is certainly hard to call this a chronic leukemia. The alternative is that the counts from July were wrong or there was a switch in the hematology lab. Any other patient have an unexpectedly high white count on July 20, 2015?

Any way, I certainly agree with undergoing a transplant, and would consider a TKI prophylactically (imatinib is the best tolerated soon after engraftment).

A 63 years-old-patient presented in August 12, 2015 with a WBC count of 39.5 Hb 13.1 and Plat 638. he had no hepatosplenomegaly and a BM aspirate had 35% myeloid blasts, 20 metaphases with t(9;22) (q34; q11) BCR-ABL p210 b2a3. He was started on dasatinib and achieved MMR4.0. Subsequently underwent a matched unrelated 10/10 PBPC transplant.
However on 20 July 2015 he had a normal PBC with 9.8 WBC with a normal differential, Hb 13.2 and Plat 449, that is 3 weeks before he presented with acute leukemia. Did he presented with CML blast crisis? Or is this Ph+ AML?
I would very much appreciate your views on this case.