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。/ [2 |( R4 E8 v1 b' a
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。( ^: l4 O+ x4 i6 D# p
& _" z, L1 ?$ m+ a: D( N* o作者:来自澳大利亚
" h& a' T7 {* N' `来源:Haematologica. 2011.8.9.( u$ a1 n3 {8 `3 M; B
Dear Group,
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/ e# }" ]# {1 l* P/ c, p BSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
$ t5 n/ A3 m. [# Y3 h/ L! k) Ktherapies. Here is a report from Australia on 3 patients who went off Sprycel4 X( U2 g" x9 \
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
) i) r. U# B1 `' J6 h/ `remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
) S7 `- o C' H8 Y# `does spike up the immune system so I hope more reports come out on this issue.( ^! q. N' ?+ d7 P% X$ F
% u6 D3 p1 f# Y* ?. @
The remarkable news about Sprycel cessation is that all 3 patients had failed
- ~) H* m. A- |Gleevec and Sprycel was their second TKI so they had resistant disease. This is% x) v O# s% B# t u; B) D
different from the stopping Gleevec trial in France which only targets patients5 a* y6 g$ v6 T* [* ?
who have done well on Gleevec.
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, I/ a, k) \% p+ W/ P/ mHopefully, the doctors will report on a larger study and long-term to see if the: S# k$ | X! e# N$ M
response off Sprycel is sustained.6 D9 m6 x- F7 x( Y1 x& H
6 D: v2 w8 }, W5 N& {0 m: M6 RBest Wishes,
) q% G8 ?. Y8 p. c7 m6 gAnjana+ w" T$ @+ `( B3 `
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$ ~+ F* C3 S( h" P1 E& f* D W2 C
Haematologica. 2011 Aug 9. [Epub ahead of print]
6 m* R$ h) B; B5 _' eDurable complete molecular remission of chronic myeloid leukemia following) G; P# E! S" }6 `% }# u1 J! O5 n
dasatinib cessation, despite adverse disease features.- f. T+ T% z8 X. f
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP., [3 X; \$ @; j9 Z( i, z+ B
Source
4 J! Q4 Q$ O- V$ c* x0 w- G9 l1 k! eAdelaide, Australia;
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1 P6 W% [( b: _Abstract
- J3 U0 S7 v3 T |/ U3 lPatients with chronic myeloid leukemia, treated with imatinib, who have a
" V3 G, Q* X; d6 e4 z# Odurable complete molecular response might remain in CMR after stopping3 R! E, {* S! h
treatment. Previous reports of patients stopping treatment in complete molecular" |" A! H, j$ J
response have included only patients with a good response to imatinib. We: {; f3 t. `' x5 c5 g
describe three patients with stable complete molecular response on dasatinib
* Q( A1 S# Z) G4 Etreatment following imatinib failure. Two of the three patients remain in
/ [ J! o0 g" ]. |5 n2 [4 K" ^5 Z% Rcomplete molecular response more than 12 months after stopping dasatinib. In$ g/ U6 s: }+ g: b
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ N" ~. s4 K; f( v) ]: v
show that the leukemic clone remains detectable, as we have previously shown in: M- b6 p& g, |$ ] i/ o
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as! t( ]% k; _2 h
the emergence of clonal T cell populations, were observed both in one patient
/ F' }3 i; Q9 }# G Y$ X6 Hwho relapsed and in one patient in remission. Our results suggest that the1 z3 O/ ]# s" P- C6 z
characteristics of complete molecular response on dasatinib treatment may be
; [/ M8 h& s6 T' `) esimilar to that achieved with imatinib, at least in patients with adverse8 x" u0 G. h. l1 }
disease features.
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