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。
" L/ V# @! G2 H: ] 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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( ^2 D4 F: B9 C; V; z作者：来自澳大利亚
7 h Q( ?- ?/ n! `来源：Haematologica. 2011.8.9.
' M3 A# p* ~, {, I6 ADear Group,5 |- r& G4 A+ i" j% S
& V& t' o, r3 L) ZSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
7 x9 g6 B* F4 J P5 b; p b7 atherapies. Here is a report from Australia on 3 patients who went off Sprycel: S- [( W4 W, j3 F
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients, ?% }0 _& m: b( a+ ?5 [! |: V
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
% z8 o5 t6 J6 a: pdoes spike up the immune system so I hope more reports come out on this issue.
8 ?. \) S# f" j" S; ?
0 _& A( m# N- ]! F8 k6 S7 b; gThe remarkable news about Sprycel cessation is that all 3 patients had failed% F, I/ v. v( _4 }, }3 ~
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
) e* [7 j2 i! a* f; u+ {# Ldifferent from the stopping Gleevec trial in France which only targets patients- o& T8 x+ S! p* {9 i6 o
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( I/ ]* _6 W2 u& A9 S/ l
response off Sprycel is sustained.6 r# \( O. T1 S# o
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Best Wishes,
1 y9 T6 \$ h* v% I- WAnjana
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0 A5 B3 F, P9 b9 `$ A/ u& ` b6 J2 A4 D% n% g
s; o9 c" [; t# p/ R; m
Haematologica. 2011 Aug 9. [Epub ahead of print]
% `4 ^& k8 ?- |( y, w4 zDurable complete molecular remission of chronic myeloid leukemia following
$ }/ j# m. J; t2 E/ b' w9 Jdasatinib cessation, despite adverse disease features.
% q0 M/ }9 m1 q- bRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP." \: Y' @: L( q# C
Source% o- w _1 V8 }5 v: B) G9 ?! x) A
Adelaide, Australia;. \. f) z: r$ o' W4 v: G; m$ w
0 [, r$ H! l% H, H7 o$ A# K( E' P
Abstract% W; E% A* R. a9 Y& e( ^( T
Patients with chronic myeloid leukemia, treated with imatinib, who have a
5 m( E7 v: r/ ?( K. F5 Bdurable complete molecular response might remain in CMR after stopping
. Y8 b+ k/ \9 Qtreatment. Previous reports of patients stopping treatment in complete molecular
. Z" S1 k8 r6 |6 W( mresponse have included only patients with a good response to imatinib. We# [! M4 _$ Q: ~: b
describe three patients with stable complete molecular response on dasatinib7 Q& G K1 {) t6 }7 M( k
treatment following imatinib failure. Two of the three patients remain in
I# M- [" s# o0 x) C1 p4 D2 hcomplete molecular response more than 12 months after stopping dasatinib. In
+ G ^- }4 `+ w$ F- b. Mthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 E9 O r) Z/ o |. W) B# _
show that the leukemic clone remains detectable, as we have previously shown in0 L1 g' V4 ]; s9 F8 k
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 U! `& s: L, Hthe emergence of clonal T cell populations, were observed both in one patient
' p/ p8 `' M1 H: t! Jwho relapsed and in one patient in remission. Our results suggest that the
7 U' l* o; [# z' scharacteristics of complete molecular response on dasatinib treatment may be# r0 |" t+ x4 E% Z0 D
similar to that achieved with imatinib, at least in patients with adverse
6 M$ a" m7 f p; T; l- N$ M" Kdisease features.2 K2 i5 @$ `3 T% u- B* }6 v
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