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。
- O9 U$ [4 S" w* b& a3 i+ v 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。5 P* F3 A9 u+ Y; X
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作者:来自澳大利亚
# }8 o( [. X+ _7 t8 Q$ ?& H0 G4 I来源:Haematologica. 2011.8.9.! ?& N Q3 }: e0 E; g, J' X
Dear Group,
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. ? |+ b. @# x" M/ s* wSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
! `' _# F7 j8 X. Q z' B, [therapies. Here is a report from Australia on 3 patients who went off Sprycel: c5 B& K/ c5 j6 Y( s
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
% L, l& j1 S! O$ z% L* i6 Iremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
7 I/ k. }* j U( X7 Zdoes 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 failed
I+ s; K5 n+ u2 R& t1 TGleevec and Sprycel was their second TKI so they had resistant disease. This is
$ x. o/ \0 i- m4 o( \' k4 Mdifferent from the stopping Gleevec trial in France which only targets patients" v# p! v% _3 y+ D
who have done well on Gleevec.
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* g- y9 I* P6 A3 w/ N% rHopefully, the doctors will report on a larger study and long-term to see if the: U9 @" C4 i* ^9 p5 r" Z
response off Sprycel is sustained.
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' X$ f1 Z- b' q4 T6 P" \/ cBest Wishes,/ v4 x+ ]+ X* g1 v4 _
Anjana% I5 E6 i+ C/ t! t6 y- ?- z
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& @, n% L t4 |Haematologica. 2011 Aug 9. [Epub ahead of print]0 P6 `9 ]+ v; E8 D
Durable complete molecular remission of chronic myeloid leukemia following
# C' G, U s6 z" u/ vdasatinib cessation, despite adverse disease features.
5 r( t1 g* b# ^$ \. B6 JRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.# `4 X+ G: a4 d+ s
Source T1 b$ _% g( U* k
Adelaide, Australia;
2 L9 {& m. ~# j1 _5 ^ d! I3 T8 J3 c7 c! p* c6 j* S1 r) o8 o
Abstract
3 L% a1 x0 n5 Z" QPatients with chronic myeloid leukemia, treated with imatinib, who have a: y" W7 `2 a* H
durable complete molecular response might remain in CMR after stopping) X& f+ U7 Y: Y4 s5 d1 b. z
treatment. Previous reports of patients stopping treatment in complete molecular+ N- n- `+ \. C8 {/ C2 x7 a
response have included only patients with a good response to imatinib. We0 P0 _3 y4 Z" F2 K3 m
describe three patients with stable complete molecular response on dasatinib+ m; N* ]. J) g8 w
treatment following imatinib failure. Two of the three patients remain in
. }) ?0 o! k" c1 n% S6 _' Ucomplete molecular response more than 12 months after stopping dasatinib. In
, ]2 _8 w, G- y- v [" p2 y7 hthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
7 [$ G* O4 m6 p" x+ jshow that the leukemic clone remains detectable, as we have previously shown in
5 y( Z. e: f9 |imatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 ?' N) W- D" L
the emergence of clonal T cell populations, were observed both in one patient
8 d, p" J7 I7 pwho relapsed and in one patient in remission. Our results suggest that the; t" y& Z. U( x$ w
characteristics of complete molecular response on dasatinib treatment may be+ P4 ]9 o S2 c, W% `7 B/ }
similar to that achieved with imatinib, at least in patients with adverse( h/ d' f" D4 {! P+ U
disease features.' o0 G1 F( c! J4 X& }4 X) q' [
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