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。
; F" F: O7 t) M6 A9 N 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
$ \3 D) z# U) Q! d T+ t* [4 Q1 T来源:Haematologica. 2011.8.9.
: b# D$ A9 i1 D4 }- fDear Group,) r6 J. u4 E1 ^/ s9 S: z$ m4 k
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML4 E9 { \% v5 P
therapies. Here is a report from Australia on 3 patients who went off Sprycel
8 `% ?" ~: R/ | yafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
) L! y( H# P) s* ~4 Rremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# U4 G! c" [- sdoes spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed
" R/ v: G* g1 t8 f/ a/ f+ X' a9 g. UGleevec and Sprycel was their second TKI so they had resistant disease. This is
6 |2 @6 q2 ^$ n3 ~5 a4 h0 K& L- t8 Rdifferent from the stopping Gleevec trial in France which only targets patients6 `- \( P+ g$ _( ?( v
who have done well on Gleevec.
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# z/ N4 ^( P' P) O7 r, Y3 Z6 m5 k* |Hopefully, the doctors will report on a larger study and long-term to see if the K9 L: b" v% G8 p
response off Sprycel is sustained.
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Best Wishes,
8 p8 `3 t' P& e( Z" tAnjana
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- Z8 ^( k d' |) L3 s; FHaematologica. 2011 Aug 9. [Epub ahead of print]6 e0 {2 C e; l. s' N" Z
Durable complete molecular remission of chronic myeloid leukemia following
; y: ~9 a6 D3 Z( N% Qdasatinib cessation, despite adverse disease features.
_* L3 A( T& ?" I, kRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
2 L$ N9 u0 {- A6 y# T& fSource
# f% ]7 c' F- y% [Adelaide, Australia;& m2 j- p( k3 ]8 C
$ J) f& q! ]# z# Q" D# ZAbstract
" N; B& \# p J, A' E8 Z9 pPatients with chronic myeloid leukemia, treated with imatinib, who have a
% {& s6 m- [. A) k% Xdurable complete molecular response might remain in CMR after stopping
9 i( Z: }% w3 b7 i4 @treatment. Previous reports of patients stopping treatment in complete molecular" i$ S+ J V& a9 F# [+ l
response have included only patients with a good response to imatinib. We. _' k3 ^( t( v5 I( x5 p
describe three patients with stable complete molecular response on dasatinib
" I* I" ?4 W& d" z7 h2 \3 \treatment following imatinib failure. Two of the three patients remain in
. A8 d) a7 W- O( A1 ]2 L; @complete molecular response more than 12 months after stopping dasatinib. In
# @" D: b, h; f! t+ W1 Xthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to `5 z1 d( S: S) ?
show that the leukemic clone remains detectable, as we have previously shown in, z3 }6 W2 ^8 i- d$ w# X
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
5 |; D# Y* |! |: }the emergence of clonal T cell populations, were observed both in one patient. B. b& R& U9 q, S, ^7 K: F
who relapsed and in one patient in remission. Our results suggest that the
' j8 ~+ \3 }/ }8 X# Echaracteristics of complete molecular response on dasatinib treatment may be
9 @5 N0 G: x2 @/ Csimilar to that achieved with imatinib, at least in patients with adverse' F: I: ]! p$ x; s
disease features.
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