This is a very unfortunate scenario and the long term outlook for this individual is very grave even with the most aggressive management such as a second allograft. As stated, there is no mention of pre-transplant IT therapy. Agreed that dasatinib is the only TKI to get into the CNS, but this in itself is probably insufficient therapy. Blast crisis CML patients should be checked for CNS disease and treated if positive with the same type of drugs that one would use for an ALL patient. Consideration of post SCT IT therapy should also be made. Unfortunately as well, this patient had what sounds like a double dose of T-cell depletion, both with the use of a T-depleted graft and the addition of ATG to the conditioning. With a disease such as CML in a young individual, where the GVL effect is so important, this becomes an issue and needs to be considered if regrafting is a thought in this individual.
Unless you can clear the CNS, then nothing will work. Personally, I would favor very aggressive management despite the toxicity potential. I would go with craniospinal irradiation at full dose and a CyTBI based regimen, where the TBI is built into the last part of the craniospinal irradiation. Regrafting should be with unmanipulated PBSCs and avoidance of any t-depleting whether ex vivo or in vivo. Early discontination of immunosuppression, say by 60-90 days, in the absence of any acute GVHD should be considered and although the evidence is weak, restarting dasatinib post allograft. Again, consideration of post allograft IT therapy is a possibility.
Despite this, the likelihood of controlling the CML is poor, but I believe anything short of this is palliative. And as mentioned by Kimmo, be prepared for major toxicity.
One last issue. Given that there was little GVH, my assumption has been that this was because of the preparative regimen and not the donor/recipient incompatibility. If a second related donor is available, again with not a lot of evidence, they could be considered.
Jeff Lipton
Toronto