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。
5 s# T: }! n" G4 Y4 j 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( D+ r! m' m% A5 L/ O: ^. w: X
来源:Haematologica. 2011.8.9.9 K2 \' f4 c9 F, o* z" z" `& ]
Dear Group,3 Q& h& ?& d) s0 k9 x
3 M3 B& A- d# x3 ?; Q. s9 I$ K nSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML; G9 c3 G2 u) u( p
therapies. Here is a report from Australia on 3 patients who went off Sprycel3 Q6 [+ b) w6 ?% [' G
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
; _+ y3 A3 P9 hremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 I9 h4 c/ J$ P% ?0 t/ j
does spike up the immune system so I hope more reports come out on this issue.
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+ B0 ` b8 ]' _, q6 H+ YThe remarkable news about Sprycel cessation is that all 3 patients had failed( N3 W3 c4 \- c5 i9 G1 {2 {
Gleevec and Sprycel was their second TKI so they had resistant disease. This is0 k' Q2 ^$ G+ q
different from the stopping Gleevec trial in France which only targets patients
5 @9 C, ~# x: O; o" x F# ?' Iwho have done well on Gleevec./ U1 E& t8 D. ?4 [) s4 R
5 [/ o* O! a1 y( H O* A: |# a0 \Hopefully, the doctors will report on a larger study and long-term to see if the
5 U0 s3 [# A" |% tresponse off Sprycel is sustained.5 ?$ z8 \* t2 S; d/ O" L
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Best Wishes,2 f' V( {8 c4 S# H5 M5 n7 E
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]% k! J; m6 u% G+ g" T) M/ C
Durable complete molecular remission of chronic myeloid leukemia following7 D2 y! m. b/ ~% A. ?, b6 ?
dasatinib cessation, despite adverse disease features.
! _9 p' G* P7 H3 c# ^Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
7 d" O1 p8 ?' b) r4 g, d2 zSource" r7 Y3 P8 W2 S" F
Adelaide, Australia;" [: B) F0 p1 g4 O$ ?, ]
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Abstract8 g" b2 l+ y9 c1 S6 f4 K8 m& T8 K
Patients with chronic myeloid leukemia, treated with imatinib, who have a
/ H7 n3 N9 W4 c4 w) Odurable complete molecular response might remain in CMR after stopping
5 |! d D, C: x0 A( a% rtreatment. Previous reports of patients stopping treatment in complete molecular
% S. q8 ]' g4 v& M2 H% tresponse have included only patients with a good response to imatinib. We
" \; g6 y/ H+ q+ ddescribe three patients with stable complete molecular response on dasatinib9 V- v) ? F2 Y) ~( O" X% U5 h
treatment following imatinib failure. Two of the three patients remain in
2 L" U7 n4 z. c, |) r# Tcomplete molecular response more than 12 months after stopping dasatinib. In
+ d% K- i$ Q1 ?+ X; |: i* kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
% O4 { n. [! Q2 j3 d/ D1 yshow that the leukemic clone remains detectable, as we have previously shown in
. \6 @( z# n0 B( A* Kimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
, @) S: R- S. S! Athe emergence of clonal T cell populations, were observed both in one patient
& z: W% J8 j7 ?, n$ Xwho relapsed and in one patient in remission. Our results suggest that the: V3 \! d0 X1 V! c
characteristics of complete molecular response on dasatinib treatment may be+ l$ z: Q8 @ u4 Z$ K8 [) q
similar to that achieved with imatinib, at least in patients with adverse
& T+ f @% e \disease features.
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