摘要:这3名患者在取得稳定的分子学缓解之后(融合基因转阴PCRU)停用达沙替尼。1名患者复发,另外两名患者在1年后仍保持了PCRU。以前说过,达沙替尼确实可以提高免疫力,希望今后能获得更多的相关研究报告。
) A- p6 |' @$ v- }' r 关于这个研究值得注意的是,这三名患者都是服用格列卫失败后转用达沙替尼的,也即他们对格列卫是耐药的。这与法国的格列卫停药研究又有所不同,那个研究中的患者都是对格列卫反应良好的。希望医生们能扩大研究长期观察,看看停用达沙替尼是否能持久不复发。
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作者:来自澳大利亚
9 V9 O. Q8 E9 i- Z. p5 a来源:Haematologica. 2011.8.9.
3 X- I# E5 Y1 I5 _2 gDear Group, i" V4 k. t6 }
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ P) ^0 C0 j4 g! Z/ {4 y
therapies. Here is a report from Australia on 3 patients who went off Sprycel
/ w* y3 M0 ~4 Eafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients' h4 G/ e; O8 t
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& G' \6 K! a( C5 x3 E+ M- l adoes spike up the immune system so I hope more reports come out on this issue.2 }! ~, o" x5 S5 s4 f6 Q! {
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The remarkable news about Sprycel cessation is that all 3 patients had failed! ~% |$ V% Q5 v6 z) f e# |; k: b
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
+ D' h Q9 B$ d& xdifferent from the stopping Gleevec trial in France which only targets patients" H" C' N8 b) ] N, l) [
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
# s1 t& ?* C4 Cresponse off Sprycel is sustained.
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5 D$ b* l: T, H# UBest Wishes,# c8 h7 W; d* W* _6 {# V
Anjana' j; x& q9 Y: t" W' q
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( ~% k8 S) }- y6 X8 N9 n) m' SHaematologica. 2011 Aug 9. [Epub ahead of print]
: d, U# T/ g% h( bDurable complete molecular remission of chronic myeloid leukemia following9 D/ o: }- ]4 }- k! G/ ^
dasatinib cessation, despite adverse disease features.
1 T9 D; D7 [% C3 d: ?5 GRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
8 y: G5 `* y8 i+ DSource
2 Y7 S( G0 o$ CAdelaide, Australia;7 F, k/ L: G' W) ` p
5 I/ B6 Q6 E* ]/ p% RAbstract W2 e% G& C: C& a; o0 @$ |6 z0 y
Patients with chronic myeloid leukemia, treated with imatinib, who have a
" ~1 O) V* u( {1 U N! F& `* J4 xdurable complete molecular response might remain in CMR after stopping: M: `: F3 x3 U0 K2 _. D w6 `
treatment. Previous reports of patients stopping treatment in complete molecular
% l4 d6 Y& a* lresponse have included only patients with a good response to imatinib. We
4 ~# ?2 V4 i$ p) L, Kdescribe three patients with stable complete molecular response on dasatinib3 z' @$ Q4 K# f/ R. @" I' _9 j5 }: Y
treatment following imatinib failure. Two of the three patients remain in+ }6 {5 B9 I8 D. V* p2 L* I
complete molecular response more than 12 months after stopping dasatinib. In |) V$ @1 @$ N+ [& c0 r( Q
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
/ A3 ~; z4 w6 S7 X; E" jshow that the leukemic clone remains detectable, as we have previously shown in
" ^3 @7 v' L$ i! `; Cimatinib-treated patients. Dasatinib-associated immunological phenomena, such as3 b! @, i- K( d+ I% p
the emergence of clonal T cell populations, were observed both in one patient
0 o# o/ m) s+ a" j& a. ]; M/ ewho relapsed and in one patient in remission. Our results suggest that the
, U/ P# d0 w( f7 E$ X9 o9 Pcharacteristics of complete molecular response on dasatinib treatment may be
% c" Z: h& m) J8 z. |similar to that achieved with imatinib, at least in patients with adverse
0 D: L) ^! `) Y; z. ndisease features.3 W5 ]3 v& L# p, q. z |
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