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。
3 ^9 C4 v( q- ^/ I' E' I2 | 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。$ f0 u9 Z5 |" f. d! V: O! G
; ]1 D5 g j! V6 Z作者:来自澳大利亚
& M, a' {6 o' H! J& ~# K9 U+ X4 P来源:Haematologica. 2011.8.9.
) ^5 X, j$ O5 ]: d3 A* X9 m4 eDear Group,
g, D. n0 Y$ U/ ~3 Y* I7 X5 q g. X3 ` b/ E3 ]
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: G$ a! a/ s1 d" k; mtherapies. Here is a report from Australia on 3 patients who went off Sprycel3 {% O+ \" Q; F H9 Y
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ f. w7 V( P9 u/ T4 [* }: Iremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel2 M2 s, w" z3 h6 a
does 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 failed6 h5 e2 [# C: r+ a" A: ~4 a. j
Gleevec and Sprycel was their second TKI so they had resistant disease. This is/ }4 Q# i6 [% [3 j4 v# Y: M o
different from the stopping Gleevec trial in France which only targets patients! |! f! I3 J# M5 Z p
who have done well on Gleevec.
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+ A4 h* S- ~; v. |: Y2 HHopefully, the doctors will report on a larger study and long-term to see if the" ?3 J3 C) k8 S& ]( [
response off Sprycel is sustained.
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- F, U# M6 p% X& j0 p2 bBest Wishes,
* ~1 n: L4 E' _0 l( Q- FAnjana
. R+ H1 K/ Z* |2 ?, m* v$ o R6 B6 ^: |# n7 e' J3 x( `0 d! l8 h* E
) d N3 s. t) e6 ~+ L
3 z' d. T: T6 S$ j T/ @0 N5 wHaematologica. 2011 Aug 9. [Epub ahead of print]
! c; E2 G2 a3 _3 TDurable complete molecular remission of chronic myeloid leukemia following$ P' A& ?' s( J2 W+ ]! `$ p9 }
dasatinib cessation, despite adverse disease features.$ L7 i) `& ^# B0 Z1 E+ P
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
8 V: N3 X) m0 n M p; ~Source) f8 \4 x$ e( z: U# k" l# ?
Adelaide, Australia;: e5 b( F4 t) ?
7 |0 ?3 F0 Y& e. |$ k6 w. T, \Abstract
' |- \/ R" C# \2 b$ w6 @Patients with chronic myeloid leukemia, treated with imatinib, who have a
% V) K! X6 \! z \* S& Xdurable complete molecular response might remain in CMR after stopping1 D6 \$ j/ P6 r/ s
treatment. Previous reports of patients stopping treatment in complete molecular
' P! L, L/ C$ Q$ Y3 q7 g' Sresponse have included only patients with a good response to imatinib. We
" Q% y$ v" r) h1 y' ?9 w: r8 adescribe three patients with stable complete molecular response on dasatinib3 Q2 a1 `/ F9 h% x( J- ]
treatment following imatinib failure. Two of the three patients remain in
" C% o: @: {5 R5 {1 ], mcomplete molecular response more than 12 months after stopping dasatinib. In/ B% M5 B: a9 l5 R7 N
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to. [* _9 ~1 m* y
show that the leukemic clone remains detectable, as we have previously shown in
r& o" j' b& q! m& H% C# E1 B% rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
* y- p% U I' R2 a* I* z* Q6 b* dthe emergence of clonal T cell populations, were observed both in one patient
" R" V0 A1 k% U* f/ ] @who relapsed and in one patient in remission. Our results suggest that the
" i0 r; c5 n, {, Q; ]4 L/ `% |2 [characteristics of complete molecular response on dasatinib treatment may be/ }: p3 \" c. E1 C* E
similar to that achieved with imatinib, at least in patients with adverse
9 L( J Y1 K* v+ Edisease features.6 p* R( {; r. u: `5 D4 Y/ T
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