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。
/ l9 W* z- X! |! t$ O7 |3 ~9 N: Q1 J c 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
' i: n! x* M5 e$ R; Q2 a) B( K; L% l来源:Haematologica. 2011.8.9.. U+ V8 S: O5 T
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" ~5 W1 G4 Y2 q! T4 Z% j( U. T1 X
therapies. Here is a report from Australia on 3 patients who went off Sprycel
4 y9 E1 ^$ \4 ~, d7 z. I( Bafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients9 X1 Z7 ~! f2 p
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel" }5 Y7 Y0 s1 b1 L! Q
does 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" I5 O& Y% W. s3 Q3 Z' F
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
: c z- h% |1 u' \0 t7 xdifferent from the stopping Gleevec trial in France which only targets patients* r8 i1 R8 W" L+ F9 V
who have done well on Gleevec./ h" O$ g" W- {
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Hopefully, the doctors will report on a larger study and long-term to see if the3 k, ^, U$ j) M2 C5 `
response off Sprycel is sustained.. ~5 t! O e3 L* s: b
- }8 _5 z/ T& s, U4 qBest Wishes,
& @" V# i3 L9 A* j, mAnjana' p; F; F' g$ Y1 z
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' S; k% d- c T1 @1 NHaematologica. 2011 Aug 9. [Epub ahead of print]
) r, F# c5 ], ]3 H/ R0 cDurable complete molecular remission of chronic myeloid leukemia following
& {+ x7 u% C) G8 Jdasatinib cessation, despite adverse disease features.' k( B1 W/ V: M% v2 q6 ^
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ B" k# d( K6 z! o" f# H8 [
Source
7 C" h8 x+ m+ C X7 ?Adelaide, Australia;2 X; u) I: M% Y7 s9 M$ c. R
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Abstract
( m$ S5 W. @9 }) c& gPatients with chronic myeloid leukemia, treated with imatinib, who have a. Q9 }' V" c @5 f- p8 d& W, O
durable complete molecular response might remain in CMR after stopping( p: g% a5 |! s+ O) d
treatment. Previous reports of patients stopping treatment in complete molecular: `3 S9 w' ^4 E' Y
response have included only patients with a good response to imatinib. We
: N3 a4 K7 a" Q6 J- L# hdescribe three patients with stable complete molecular response on dasatinib: ^* I* [0 }7 }0 V l7 z" C% e
treatment following imatinib failure. Two of the three patients remain in5 @: M$ n+ l' g" _' g/ b* e
complete molecular response more than 12 months after stopping dasatinib. In
& s; z" g# c. d. lthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ s0 ]% j& K* q
show that the leukemic clone remains detectable, as we have previously shown in3 z5 R/ m& L% j' N% E1 ~
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
2 R7 w( P4 y- w$ e# Jthe emergence of clonal T cell populations, were observed both in one patient7 e8 }# n( @9 B% U3 r, v
who relapsed and in one patient in remission. Our results suggest that the2 \) \" B4 `* J+ F
characteristics of complete molecular response on dasatinib treatment may be
6 N' U1 W/ |1 Zsimilar to that achieved with imatinib, at least in patients with adverse; b! I8 _5 i2 ~1 l
disease features.
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