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。
+ C+ Q& n# B7 c6 P- ^9 j 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。6 W' a# y$ M5 C5 e9 m0 E9 Y
$ q' k0 g1 P- A8 S! H作者:来自澳大利亚
0 `# [; z0 { \1 I$ |来源:Haematologica. 2011.8.9.7 l# b) k/ l& j6 H3 i4 x6 Q
Dear Group,
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- w8 m; B& f9 J1 ESome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
4 P# D8 x6 w7 T- A6 U$ |therapies. Here is a report from Australia on 3 patients who went off Sprycel
( L. N3 t# q( M2 u( P0 Aafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients* n) s: t0 e0 ^1 I& j
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
! m7 q6 O3 P# G7 I! fdoes 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
+ q9 C4 ]/ c7 EGleevec and Sprycel was their second TKI so they had resistant disease. This is! a! ^! C W0 F5 Q3 V. I W$ \
different from the stopping Gleevec trial in France which only targets patients+ U! O/ G0 J" Y/ [! O. N
who have done well on Gleevec.
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& i- Q. o) ^/ X1 v! {* `0 HHopefully, the doctors will report on a larger study and long-term to see if the$ A. @- |+ \; v/ @! [2 x8 R
response off Sprycel is sustained.3 S2 b/ A9 N* E: z& M% u) Y
8 I3 Z8 k9 h9 W6 `Best Wishes,3 o8 ^6 x7 t% I8 x8 r
Anjana) Z5 k. M3 E1 L5 Z( w' @
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" P6 g v- _0 u5 y' RHaematologica. 2011 Aug 9. [Epub ahead of print]& l& }% i! v$ `0 A
Durable complete molecular remission of chronic myeloid leukemia following2 ]* {4 O3 @- J5 T4 c% I
dasatinib cessation, despite adverse disease features.
* {& W% @* m. B9 TRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( n1 H$ R9 {! y: p: ?
Source
& I; R$ N/ w) YAdelaide, Australia;' n A- A9 `# v1 R* Z- D
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Abstract
# a1 V0 u( o8 M1 u# J! VPatients with chronic myeloid leukemia, treated with imatinib, who have a
! m& X& Y1 |/ X6 @durable complete molecular response might remain in CMR after stopping
6 z" y0 R: h: X' @) d) s0 `. a+ dtreatment. Previous reports of patients stopping treatment in complete molecular' f$ m/ q6 T) V6 E+ I* S6 P5 M
response have included only patients with a good response to imatinib. We
4 u N0 Q& j) T: I# ]; {describe three patients with stable complete molecular response on dasatinib
6 j' f% S3 A; C# E0 Z( U7 etreatment following imatinib failure. Two of the three patients remain in. X; {9 L+ `1 l
complete molecular response more than 12 months after stopping dasatinib. In2 e* J0 q/ P: i5 E2 H1 i2 n; c1 h
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to* E/ ^' X: s: ?( X
show that the leukemic clone remains detectable, as we have previously shown in
# u/ ?0 B, {1 Timatinib-treated patients. Dasatinib-associated immunological phenomena, such as
% [6 x- b! O4 c' U6 athe emergence of clonal T cell populations, were observed both in one patient
* V2 n3 N" c; ?$ [! n7 Cwho relapsed and in one patient in remission. Our results suggest that the" O6 D# F/ `4 h
characteristics of complete molecular response on dasatinib treatment may be, }& M- o$ r1 {- w; W1 F+ h4 ~
similar to that achieved with imatinib, at least in patients with adverse7 E# \. W* ^- ^7 O
disease features.
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