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。
: b: {* s9 F' c) u 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。% H3 {) k9 X, d& }8 m8 ^
3 ~2 n6 _- N8 O$ Y; o作者:来自澳大利亚! K! T1 @- A0 Y+ Y4 Z
来源:Haematologica. 2011.8.9.
+ h Y- d0 {3 D' f* Q) ODear Group," C7 |5 _3 \0 s4 g2 O8 f+ a% X
5 j o( Y% |; g8 j+ Z" x: @
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" d7 p5 G) F5 s* b# @9 Z% b1 j% u
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 g) G( H) v, J7 W: r
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients& E: v2 u! K0 S/ x
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
0 i2 y3 }6 h! @) i8 ^8 D. q: k sdoes spike up the immune system so I hope more reports come out on this issue.
9 o* g, C; g" v+ F; d! m
. b0 ^0 Q& i" A' C% BThe remarkable news about Sprycel cessation is that all 3 patients had failed6 ^* I* T! o9 y
Gleevec and Sprycel was their second TKI so they had resistant disease. This is: l9 W6 V1 o- W. L% D* ]
different from the stopping Gleevec trial in France which only targets patients
4 X2 ?& {: s) V8 D9 Qwho 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
. x0 M% E" b% X" l7 d* ]; oresponse off Sprycel is sustained.4 P9 y0 D3 E# x3 _$ D+ p
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Best Wishes,: k, @) k2 Y# g2 k6 O- V4 C$ J
Anjana0 E. @. i* Q, t% n0 r6 Z; r
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& A. n8 W0 l# ?" i
Haematologica. 2011 Aug 9. [Epub ahead of print]1 u" Z/ T( w C1 v! S
Durable complete molecular remission of chronic myeloid leukemia following& O$ m& K$ N; \- _$ g* J' l
dasatinib cessation, despite adverse disease features.
7 z% _4 N. i [! g# P, D! URoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.& @3 i+ |0 \0 s
Source' b$ o- P0 S* d: }# [( f' D
Adelaide, Australia;, H8 v9 c5 P* {/ z
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Abstract
1 y; {! L A% A% i% dPatients with chronic myeloid leukemia, treated with imatinib, who have a
% Z' O0 u% s" m( ?* idurable complete molecular response might remain in CMR after stopping# \, y6 Z1 H8 p! R* ]# U
treatment. Previous reports of patients stopping treatment in complete molecular
9 F( U& Q A# m# H! z yresponse have included only patients with a good response to imatinib. We) {1 V* j. H5 _7 k3 G6 [$ U4 U
describe three patients with stable complete molecular response on dasatinib
7 `% ^1 W% x( A5 ?2 Vtreatment following imatinib failure. Two of the three patients remain in! G/ l, M t2 h8 e' q* v
complete molecular response more than 12 months after stopping dasatinib. In
9 z4 M( I c& |$ B8 g* D/ F4 F: ethese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
! \# x* j' a" _- c: o" I7 Cshow that the leukemic clone remains detectable, as we have previously shown in5 ^5 e1 O6 f3 a# K' O
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
: f; _3 p" i3 D. F& B5 L8 ^the emergence of clonal T cell populations, were observed both in one patient( ~' ^6 r+ T- h# z' q; t
who relapsed and in one patient in remission. Our results suggest that the6 u6 O8 N* L+ D6 v( d! T
characteristics of complete molecular response on dasatinib treatment may be" H9 n1 j+ w2 Z8 g7 O# N8 ?8 K
similar to that achieved with imatinib, at least in patients with adverse
; \) Z$ \% H! ~1 t& jdisease features.5 {# \$ M1 S0 g' q* `# |8 }
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