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。7 q$ y6 w3 y. |, P0 D |
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7 G5 W9 T; F# X+ k" a5 R
来源:Haematologica. 2011.8.9.6 H& P; N0 g" p2 s* u: E
Dear Group,
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! _5 o" G5 a, f5 m! a$ \2 HSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML$ V# ?1 L8 T' n( ^1 O5 u8 G+ ^
therapies. Here is a report from Australia on 3 patients who went off Sprycel
" t7 _1 L/ @1 J9 zafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
8 B5 ?6 y5 Y! gremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel* k6 t0 l t8 C# f( g
does spike up the immune system so I hope more reports come out on this issue.& b8 h" Z' j; B5 ]& C
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The remarkable news about Sprycel cessation is that all 3 patients had failed: d+ m/ M% s) E2 o0 {. q
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
+ r( F$ w) O% g$ K1 b2 s- Ldifferent from the stopping Gleevec trial in France which only targets patients* q# [* C8 |0 z
who have done well on Gleevec.
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5 o: M1 L: w; |. a1 DHopefully, the doctors will report on a larger study and long-term to see if the
$ G% r8 Y7 \1 \6 S$ Nresponse off Sprycel is sustained.' n& z5 U1 r8 b! Z0 E0 |& A
! @8 @( b: Z9 r4 H5 ]. M- G- v+ ]" bBest Wishes,% Q8 [( W8 V+ F; X; F. y# F0 W/ r
Anjana9 P r( H/ L0 E. b" k' Y
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1 u! H; x. B* x- a7 LHaematologica. 2011 Aug 9. [Epub ahead of print]
( X8 f# F2 N& f" \/ f$ HDurable complete molecular remission of chronic myeloid leukemia following
! w8 z: O; k, ^2 Idasatinib cessation, despite adverse disease features.+ S6 u* R7 B7 }) ?
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
8 q! F5 f. d0 {- Z d+ @3 NSource
/ I2 b1 {% `# X- |% HAdelaide, Australia;
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Abstract
; ]" p& E8 [2 ?7 n6 Q* f8 ^. HPatients with chronic myeloid leukemia, treated with imatinib, who have a! X7 f# |6 G+ T
durable complete molecular response might remain in CMR after stopping
5 u. `. ^0 E3 n- h& Otreatment. Previous reports of patients stopping treatment in complete molecular
% h" Z! q, V/ r- L" Sresponse have included only patients with a good response to imatinib. We6 ]! @7 e4 t1 K9 y
describe three patients with stable complete molecular response on dasatinib
9 y. ~ t! E! R9 \$ ?$ D/ O+ Z# otreatment following imatinib failure. Two of the three patients remain in8 U% |6 j. @; R
complete molecular response more than 12 months after stopping dasatinib. In
0 u0 S3 u* ^9 b, ^, I' V0 ?7 Vthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* P( [, Z D) }# W# ]. ^show that the leukemic clone remains detectable, as we have previously shown in
8 Z1 b$ U( x0 q0 X& dimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 B: z; C! d9 n$ }' _) h' K' bthe emergence of clonal T cell populations, were observed both in one patient
& S+ p& ]+ K( s. v( \, o" W5 ~4 O! ?who relapsed and in one patient in remission. Our results suggest that the
9 b! c+ R! u- K% X% m. Q, g8 Acharacteristics of complete molecular response on dasatinib treatment may be8 A6 L, O% q! r0 Y0 M H
similar to that achieved with imatinib, at least in patients with adverse
8 n' [" B- m- Z9 c$ Y# L- cdisease features.
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