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。
7 ]' Q9 y. |: O; X3 X* T/ O 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。2 x' q. V C" j- _
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作者:来自澳大利亚
% M/ G6 t* a: D6 v8 U1 H4 d7 L来源:Haematologica. 2011.8.9.
! ?/ k& q' ?/ H+ Z7 v2 r# rDear Group,
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9 P8 ^. p; D, e' `Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML# e' m8 N5 S$ e1 y
therapies. Here is a report from Australia on 3 patients who went off Sprycel, q: X/ x% w/ H# O
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients* H. h& r9 v$ v, @
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
6 D8 T& o- [/ e. f1 ^ c* x+ ]does spike up the immune system so I hope more reports come out on this issue.
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7 n: s6 Y9 ^6 X/ F, B+ ` rThe remarkable news about Sprycel cessation is that all 3 patients had failed# @- s g% R" \# o- [3 N) b4 S% O+ c
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
# R, q% G; m- e2 rdifferent from the stopping Gleevec trial in France which only targets patients
+ H0 \' p7 }& w1 Jwho have done well on Gleevec.) r6 a* X- ?+ A( j7 N
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Hopefully, the doctors will report on a larger study and long-term to see if the! C; P7 O, x9 b7 ~. C0 y8 B' ?
response off Sprycel is sustained.- v& r( l" q! M( d/ [
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Best Wishes,4 G* L8 L- R) j$ a/ r
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
- i+ m5 R. m' T# g5 WDurable complete molecular remission of chronic myeloid leukemia following. y5 \; Q5 V/ n9 c
dasatinib cessation, despite adverse disease features.
# |7 u* g8 w: HRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP./ i) \% [- n: `4 R- x: [8 s4 p
Source' J' e2 [" C9 D/ n0 S6 T7 S2 t
Adelaide, Australia;9 d! S3 l' p+ e; Q. z
1 F& H, {# {. a# O( IAbstract
- i% b. ^" c/ [. OPatients with chronic myeloid leukemia, treated with imatinib, who have a& U3 ?1 X* N# x Q5 k; z: T/ ~
durable complete molecular response might remain in CMR after stopping
8 ]4 m) I2 K4 M& U& k6 Atreatment. Previous reports of patients stopping treatment in complete molecular
?" q- c8 j9 P3 ^- \response have included only patients with a good response to imatinib. We
6 Z" Z* y3 V/ ?2 adescribe three patients with stable complete molecular response on dasatinib
# l+ r. J5 ?$ u! `treatment following imatinib failure. Two of the three patients remain in8 S1 Q' f' M( v! } @4 K
complete molecular response more than 12 months after stopping dasatinib. In8 o: C* b, R( {5 [+ H% |
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 ?, u$ S2 B: p4 l' A$ @* z
show that the leukemic clone remains detectable, as we have previously shown in
1 t( ^8 b+ |) x% [imatinib-treated patients. Dasatinib-associated immunological phenomena, such as) ?( k0 k. X. r% `4 Q8 x. I
the emergence of clonal T cell populations, were observed both in one patient
* z9 _' {5 T2 s6 ~2 J, T6 }who relapsed and in one patient in remission. Our results suggest that the4 ?5 k0 r; u* H
characteristics of complete molecular response on dasatinib treatment may be& ~( C6 q' v5 _
similar to that achieved with imatinib, at least in patients with adverse
. J% V6 j B1 u3 @. t/ S1 @disease features.
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