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。: ], J9 m$ A5 }/ D* i; i
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。% c0 u, Y3 \4 y' F) m) d
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作者:来自澳大利亚
& s$ B1 t* E4 \$ ] b2 a$ {4 i来源:Haematologica. 2011.8.9.
) C+ D; g( T6 u$ b1 X7 a6 [Dear Group,5 @" @5 ?) B+ ]. {
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
) A$ g4 _ g) N# n* ntherapies. Here is a report from Australia on 3 patients who went off Sprycel" X; r8 x( v3 }: C
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients9 Z1 r8 L9 S4 k! g
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
3 Q% i0 v$ I idoes spike up the immune system so I hope more reports come out on this issue.4 v5 w$ s/ V8 s( [7 E
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The remarkable news about Sprycel cessation is that all 3 patients had failed
& O4 \& c" x% K& h6 LGleevec and Sprycel was their second TKI so they had resistant disease. This is
! W. D+ ^+ P/ r {/ M2 A& V# h- }different from the stopping Gleevec trial in France which only targets patients7 d, {$ ~ _: N' U: d+ c0 J
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 the4 }1 u8 }1 w( o& I) K2 m0 }
response off Sprycel is sustained.5 t: }- Y) m# \+ {2 S
2 Z* \. k) m4 TBest Wishes,0 N' Y! M3 s1 s! B
Anjana
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5 h& W, l! v2 c3 o' O# Y0 MHaematologica. 2011 Aug 9. [Epub ahead of print]1 n1 `+ w- D8 O k A* |
Durable complete molecular remission of chronic myeloid leukemia following
9 \4 W- \* K+ t. x0 ldasatinib cessation, despite adverse disease features.
5 [% x" Z" b, {" z4 b3 y2 JRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 u5 `& i0 D4 X# A0 A
Source n' b0 j8 `/ T4 J$ X" U- j7 M# y: r
Adelaide, Australia;7 l# P# I% D5 W: X2 x
$ i" ~9 g: a Z: o# nAbstract
- |' k1 n6 i4 h; L @: g2 WPatients with chronic myeloid leukemia, treated with imatinib, who have a
* V% e% }4 U+ I; R2 O) i* Ndurable complete molecular response might remain in CMR after stopping' q' J0 j' @" |; K* n+ ~9 E
treatment. Previous reports of patients stopping treatment in complete molecular
) i4 p/ a. [* ^7 R; H) C" j6 D5 Eresponse have included only patients with a good response to imatinib. We& ~: E) K: ?& b0 c8 Z
describe three patients with stable complete molecular response on dasatinib
4 M; z% ~" o4 T4 G: ktreatment following imatinib failure. Two of the three patients remain in) I6 w0 [' b% ]" p8 \
complete molecular response more than 12 months after stopping dasatinib. In
5 w2 G! |. C) E8 H0 c, K6 ?! Qthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
( e. v- b3 H- [% H4 ^8 {show that the leukemic clone remains detectable, as we have previously shown in
4 X( e4 ]" @; Z+ Qimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
3 v+ E2 J5 V- M( u( athe emergence of clonal T cell populations, were observed both in one patient
5 a0 i/ d3 @% A7 X+ T' Zwho relapsed and in one patient in remission. Our results suggest that the
6 B& M# W% J6 r. G% Hcharacteristics of complete molecular response on dasatinib treatment may be8 N; F; s4 d6 V
similar to that achieved with imatinib, at least in patients with adverse
( n" w! v$ G4 d" C- m' r/ Ndisease features.
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