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。
! m& z. b0 W% x! M: Y' 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。
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# F2 k; T7 o% F3 y7 M" L1 z作者:来自澳大利亚; Y9 G6 t- A+ g( G+ R
来源:Haematologica. 2011.8.9.& V7 o' A" u3 c# R! I
Dear Group,
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3 ]. k; b' D }. o8 [Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" G& v+ w4 Y( \/ u
therapies. Here is a report from Australia on 3 patients who went off Sprycel
9 o/ j0 r9 B7 ^ H7 Y, Bafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
) q: d( W7 B4 ~1 n& c+ n2 @remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
6 X) T# i G& a; idoes spike up the immune system so I hope more reports come out on this issue.
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8 n% s3 y) x K* c. a& R4 D4 h% GThe remarkable news about Sprycel cessation is that all 3 patients had failed
/ e4 a1 u7 J+ b- L+ f. Q/ pGleevec and Sprycel was their second TKI so they had resistant disease. This is
/ V# \& b. Z- R8 udifferent from the stopping Gleevec trial in France which only targets patients
0 m7 n: z, J1 S2 d6 l+ mwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
8 L0 g1 G3 u. F( q7 Vresponse off Sprycel is sustained.
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Best Wishes,
" z: D6 j1 w) O! tAnjana% Y/ w1 s4 N- e* Q7 d
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Haematologica. 2011 Aug 9. [Epub ahead of print]; K' I; L. B4 v3 K0 V
Durable complete molecular remission of chronic myeloid leukemia following, g5 M6 N9 a6 b) T& {
dasatinib cessation, despite adverse disease features.
0 s/ k* U C1 BRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
5 C: P1 U$ z! H+ [Source
4 B Q9 Z% X8 [. S% bAdelaide, Australia;
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F; X6 Q: {6 B3 C& o( SAbstract
/ V' B9 D% F! d% i3 K7 o( wPatients with chronic myeloid leukemia, treated with imatinib, who have a
4 n9 ~( [! P$ k: Z2 ~durable complete molecular response might remain in CMR after stopping
) P o- z$ A0 t- f3 x: @- atreatment. Previous reports of patients stopping treatment in complete molecular
' X# q1 h2 W, X: t$ A' d) Sresponse have included only patients with a good response to imatinib. We
# s/ Y! u+ a/ n" Y! i5 idescribe three patients with stable complete molecular response on dasatinib
7 b: b, N) @! Vtreatment following imatinib failure. Two of the three patients remain in0 |8 D* I% ?0 {) o) L) `( r; g
complete molecular response more than 12 months after stopping dasatinib. In
9 i& Y W5 Z, }6 N* |these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
o7 e/ S' d9 S* q1 d$ Y0 [show that the leukemic clone remains detectable, as we have previously shown in
6 |& r, {7 _; m6 _' x% j- limatinib-treated patients. Dasatinib-associated immunological phenomena, such as
. R" D& s& x# p% m) ]/ Fthe emergence of clonal T cell populations, were observed both in one patient
* ~7 D" i' T4 {: F5 [. y7 {2 } v) Owho relapsed and in one patient in remission. Our results suggest that the) ~. L" T8 Q. v" \: p* A
characteristics of complete molecular response on dasatinib treatment may be
% e2 E4 r1 A' Q T2 e6 Qsimilar to that achieved with imatinib, at least in patients with adverse
% F" p( x$ m- j8 _& b* t5 {8 `disease features.8 h; c1 Y+ F; c3 `2 T; p6 w7 b
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