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。
- r1 o' O3 I" d' Q4 }7 Q 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。* l( E$ E$ Y3 C
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作者:来自澳大利亚
/ P6 M; R3 G* M. G" r8 _& \0 J5 X( D来源:Haematologica. 2011.8.9.# Z9 p0 E4 _" w( ?2 P7 x
Dear Group,3 i0 i( y3 ?) Y6 ^6 A; Y
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
$ p& V6 `( W8 w+ Ftherapies. Here is a report from Australia on 3 patients who went off Sprycel' e8 I, N, A7 t7 H' L! _
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients! E; D) J: }: Y y
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
! X2 `$ q- A6 j( C6 G9 j1 s/ Vdoes spike up the immune system so I hope more reports come out on this issue.# j! G# W; W) W- N4 T9 e# p
/ u, @: m* F& z, l8 Z( f& qThe remarkable news about Sprycel cessation is that all 3 patients had failed
2 \ I% P9 J4 RGleevec and Sprycel was their second TKI so they had resistant disease. This is6 m/ [3 n; Q, J8 ~' p- w8 p) ^: {
different from the stopping Gleevec trial in France which only targets patients( k7 k W( `* `9 T5 A% [: o9 n) I' v
who have done well on Gleevec.
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" t/ C/ a" r3 @5 {! i) q7 s2 DHopefully, the doctors will report on a larger study and long-term to see if the
# B& ?* E1 f2 \ U/ Vresponse off Sprycel is sustained. K4 J9 {/ H+ I7 p
2 p' Y2 V G( T2 qBest Wishes,
6 p* u4 f. p! \ TAnjana9 k2 F1 G. B% Q0 ]
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Haematologica. 2011 Aug 9. [Epub ahead of print] N$ k/ U5 Q! e# p, j6 N7 ~
Durable complete molecular remission of chronic myeloid leukemia following- w/ y1 i; K- d6 m# K1 Y
dasatinib cessation, despite adverse disease features.$ L2 M' W3 @* _- g3 Y
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
# B) o& A4 _% a) lSource
% B9 L4 l1 }& s3 tAdelaide, Australia;
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Abstract7 `# N1 I% `% J7 a. I: [
Patients with chronic myeloid leukemia, treated with imatinib, who have a( I& {& V: x9 O5 Z
durable complete molecular response might remain in CMR after stopping
0 b3 e7 a- }9 X: Jtreatment. Previous reports of patients stopping treatment in complete molecular3 C6 d& q6 l* x, D2 ?
response have included only patients with a good response to imatinib. We
& l5 B6 d( _ o8 }" s/ y; Qdescribe three patients with stable complete molecular response on dasatinib
5 M. Y( b: {) A5 I6 B5 Ttreatment following imatinib failure. Two of the three patients remain in
; W% a& w6 s7 s% ^complete molecular response more than 12 months after stopping dasatinib. In
. L' d" p+ L! l- x1 Z! A! z8 Lthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& e: ?) _3 b3 g7 f+ q+ a' G
show that the leukemic clone remains detectable, as we have previously shown in
8 g" Z/ L0 U- x+ c j0 \imatinib-treated patients. Dasatinib-associated immunological phenomena, such as3 g6 j, f( |% ?3 L) N2 s1 M
the emergence of clonal T cell populations, were observed both in one patient8 N( o( K& r X5 Y: _+ l# R8 H
who relapsed and in one patient in remission. Our results suggest that the
6 l4 a: |- `+ G$ w9 j D/ [! `characteristics of complete molecular response on dasatinib treatment may be& H6 C* q/ }9 W
similar to that achieved with imatinib, at least in patients with adverse4 a3 {9 A/ L6 U V
disease features.& v! O8 W4 c- {$ ^# y
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