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Reply: CML intolerant/resistant to all TKIs


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Topic History of: CML intolerant/resistant to all TKIs

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11 years 1 week ago
Re: CML intolerant/resistant to all TKIs

Some patients require significant dose reduction for pancytopenia when the issue is multi-drug intolerance. For instance, some patients have responded to dosage as low as 20mg dasatinib, which has allowed continuous drug therapy and also marrow recovery. Dr Cortes at MDA can consult on this.

Trey
CML Patient Advocate
USA

  • Pankaj Malhotra
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11 years 1 week ago
Re: CML intolerant/resistant to all TKIs

This additional information is very useful. Information on bone marrow cellularity, number of blasts, presence of myelofibrosis and type of BCR ABL transcripts and presence of any co-morbidities in the patient would be highly appreciated.

11 years 1 week ago
Re: CML intolerant/resistant to all TKIs

Some additional information: He has no detectable BCR-ABL mutation. He has been on TKI therapy without interruptions, at reduced doses of the TKIs because of the cytopenias (dasatinib 100mg then 70mg a day; nilotinib 300mg BID then 150 mg BID; bosutinib 300mg a day; ponatinib 15 mg a day.)
David Snyder

  • Giuseppe Saglio
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11 years 1 week ago
Re: CML intolerant/resistant to all TKIs

It is reasonable to try also with imatinib as suggested by Michele (just in case) and with the help of growth factors, but it is unlikely that a patient resistant/intollerant to 3 different TKIs (including ponatinib) will respond. So I think that the only available option will remain allo.

Beppe Saglio

  • Jerald Radich
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11 years 1 week ago
Re: CML intolerant/resistant to all TKIs

D,

I would probably go with an allo. If you have a research protocol for NMA, or if the gent has tons of toxicities, NMA would be be fine. We would probably opt for a full with targeted bu-cy, since we (my paper, Blood) didn't show any survival difference with ages up to 65 yrs.

J
Jerald Radich, MD

  • John Goldman
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11 years 1 week ago
Re: CML intolerant/resistant to all TKIs

I think that a trial of imatinib along the lines suggested by Michele Baccarani is reasonable though I agree with the suggestion that he probably has an unusually small residual population of Ph- cells and may do equally badly with imatinib as with other TKIs. I would certainly move slowly in the direction of SCT with the best available donor and probably use RIC – with the intention of supplementing this with DLI when necessary.

Not sure that this helps very much

John Goldman