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。
: d3 m9 x5 |" } 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; m# K O" j1 Y- M+ p1 f$ [
来源:Haematologica. 2011.8.9.1 `8 U8 g# z! \4 S
Dear Group,
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! o" y* p. J* eSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML, z5 q0 F. g7 s7 m) ^& ~
therapies. Here is a report from Australia on 3 patients who went off Sprycel' M2 k. }! I2 g: K/ n- K j
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ `4 K" j8 U# D5 Z" W1 |+ Jremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- ?0 c) J. h- P; x) mdoes spike up the immune system so I hope more reports come out on this issue.
+ S8 [: W/ O: k. N9 ^) t5 x+ [6 `
/ O e. G6 S: Q' _) w7 b" p& @The remarkable news about Sprycel cessation is that all 3 patients had failed: g2 S' Q: K- N5 f
Gleevec and Sprycel was their second TKI so they had resistant disease. This is6 o! s8 w/ [' E% Q
different from the stopping Gleevec trial in France which only targets patients
8 d) I2 V5 p) @( v. Dwho have done well on Gleevec.' n- c/ x3 a( i/ W& P
% j, J5 I" t7 G8 K; J7 j7 P- YHopefully, the doctors will report on a larger study and long-term to see if the
' ]- X0 i2 ^/ Z+ M2 V; _' v+ Q0 Rresponse off Sprycel is sustained.
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. g5 n4 O' B! @8 L! V! c0 v6 ZBest Wishes,2 ~# U% j1 W% b) J0 T
Anjana- t3 m3 Q. j$ V- W
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Haematologica. 2011 Aug 9. [Epub ahead of print]6 w) v [: T& D1 N
Durable complete molecular remission of chronic myeloid leukemia following
2 v8 O' W1 H. S6 _+ ^- b7 y7 x% {dasatinib cessation, despite adverse disease features.) y, ], H8 n* O7 d. W
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;. G) b! E6 l6 V1 {$ L6 n5 x
) w3 n7 }1 Z4 l; p2 Q5 T. N' BAbstract% j6 v) _# ~2 A' }( v( [
Patients with chronic myeloid leukemia, treated with imatinib, who have a" @; H" P2 u% a1 S) `; K
durable complete molecular response might remain in CMR after stopping
7 k7 L# @. ^' v# {; j; [4 q( ytreatment. Previous reports of patients stopping treatment in complete molecular3 A% c7 g! E# {* ?: }: \* U( T5 U
response have included only patients with a good response to imatinib. We
0 D8 U5 }7 M" o! a5 qdescribe three patients with stable complete molecular response on dasatinib6 g- \: Z& ?2 }% N1 Y
treatment following imatinib failure. Two of the three patients remain in
5 X( y8 D' L% z2 L/ M) k1 ?1 dcomplete molecular response more than 12 months after stopping dasatinib. In
# f: D# `- T3 I' e9 l& ]these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* v+ E/ _6 l# `: e# e' Bshow that the leukemic clone remains detectable, as we have previously shown in- ? u1 _8 k* y7 n1 d) a' b1 }
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
2 \+ ~" [9 Z' [8 U+ zthe emergence of clonal T cell populations, were observed both in one patient
; i3 r; ]" Q: }! K! i! ]7 gwho relapsed and in one patient in remission. Our results suggest that the# I- K5 P1 M/ h- F" Z! ~1 H, h
characteristics of complete molecular response on dasatinib treatment may be
/ @. w$ |) i4 b$ Jsimilar to that achieved with imatinib, at least in patients with adverse7 J) ?. i# t( t' Y
disease features.
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