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Reply: CML-CP, high risk failure to respond to imatinib


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Topic History of: CML-CP, high risk failure to respond to imatinib

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  • Franck NICOLINI
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11 years 3 weeks ago
Re: CML-CP, high risk failure to respond to imatinib

The absence of the variant Philadelphia chromosome at diagnosis is odd.
However this is a cytogenetic failure at 3 months after IM 600.
I would certainly search for a sibling or unrelated donor now.
I would increase Dasatinib at 140 mg daily and if not suitable response would transplant the lady if no comorbidities and proper donor

  • Michele Baccarani
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11 years 3 weeks ago
Re: CML-CP, high risk failure to respond to imatinib

My suggestion is to continue Dasatinib, to monitor the molecular response monthly, and to activate immediately the search of a family donor. Once a suitable donor is found, I would transplant, unless the BCR-ABL transcripts level falls rapidly (within three months) to less than 1%.
Best regards, Michele B.

  • Hilda Mangos
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11 years 3 weeks ago
CML-CP, high risk failure to respond to imatinib

I would be grateful for your advice in the management of a patient, aged 47, who’s variant t(9;11) by FISH in her BMA is 36.5% (73/200 cells) and her BCR/ABL in her BMA is 37.600 three months post Dasatinib 100mg daily, but six months from diagnosis (three months on Imatinib 600mg).

Patient history
Chronic myeloid leukaemia, chronic phase (CML-CP) – August 2012
Sokal score 2.82 (High),
Hasford 1564.28 (High),
EUTOS score 113 or high risk group, EUTOS probability for no CCgr 0.27

Aug 12 - PB% =321.000, BM karyotype 46,XX,t(9;11)(q34;q13)[20]*
Imatinib 600mg
Oct 12 - PB% = 37.300
Nov 12 - BMA % = 69.500, BM karyotype 46,XX,t(9;22;11)q34;q11.2;q13)[20].
Imatinib 600mg ceased 6th Nov, Dasatinib 8th Nov, Dasatinib 100mg daily Nov 2012
Feb 13 - BMA % 37.600 BM FISH 73/200 36.5%

Medications: Dasatinib 100mg daily

Blood results: Hb 118, WBC 9.3, Plts 244, N 2.5, Lymph 6.,creat 101, ALP 16, GGT 9, calcium 2.4, magnesium 0.8. PBF reactive lymphocytes (viral illness in Dec)

She has achieved almost normal haematological values, her splenomegaly is not longer palpable, has no side effects on Dasatinib and compliance to her medication is excellent.

Her TK mutation studies did not detected a mutation.

The questions I have are:
Do we continue Dasatinib in the meantime with monthly BCR/ABL’s?
If so, what parameters of response should I follow and what alternatives of treatment are advisable?

Do you think HLA typing from her siblings would be advisable at this stage?

Dr Hilda Mangos
Southland Hospital
New Zealand