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。4 g6 Y4 q! g4 g- w4 |2 {. I
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。' i- s. [1 T& s) A+ |
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作者:来自澳大利亚
6 V4 F4 l% D* k9 H o来源:Haematologica. 2011.8.9.1 R: P* E9 l5 y- }. p
Dear Group,% m' U5 U/ v/ h K* ~( Z" n
! w/ ^% F( p, s9 q; aSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML1 a {+ N6 ^1 N
therapies. Here is a report from Australia on 3 patients who went off Sprycel
* ]1 R2 U: s! u: K6 mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
% z( c$ U( b5 d1 oremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 ^) l/ G" ?- D! l. pdoes spike up the immune system so I hope more reports come out on this issue.2 l! r& w: ?% [. @
8 E9 J r3 h# ]- v2 n9 j; BThe remarkable news about Sprycel cessation is that all 3 patients had failed
+ {# E; i7 N4 w* g" gGleevec and Sprycel was their second TKI so they had resistant disease. This is
4 v$ `- \" H4 u* c# odifferent from the stopping Gleevec trial in France which only targets patients
& [# U1 y: @3 O/ |( ]who have done well on Gleevec.
8 {5 p8 v; N4 d- l& }
8 N! k+ b* s) e- @ P6 [& IHopefully, the doctors will report on a larger study and long-term to see if the! {2 ^: V$ j2 j+ ?/ ]+ q0 U
response off Sprycel is sustained.
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8 f7 j3 R% [+ ?7 N5 I* ^0 dBest Wishes,5 M- J& x( Q( `( ~" D
Anjana
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& U% G! L0 ^' C
. Z4 R' x8 [' cHaematologica. 2011 Aug 9. [Epub ahead of print]
; U' I- Y' X' \$ xDurable complete molecular remission of chronic myeloid leukemia following1 A6 U3 t' i% u6 I6 R/ a
dasatinib cessation, despite adverse disease features.: o8 Z+ s6 F$ t( S- V
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.2 q- r( m$ _0 @8 i, f2 _! U0 B
Source
! A7 ]6 t8 C) @/ jAdelaide, Australia;# @" \- k9 `' h/ z4 p% h" s( t) x
0 n; p& ], m2 s4 G( Y0 H# U8 y4 gAbstract
0 Q8 s! O2 F$ R* JPatients with chronic myeloid leukemia, treated with imatinib, who have a* Y0 C9 |5 ^; u# t
durable complete molecular response might remain in CMR after stopping
& {! A* w* I& ]3 |! |1 S" v/ l0 vtreatment. Previous reports of patients stopping treatment in complete molecular; G+ `" q9 p+ z t' N/ |2 V- o* x
response have included only patients with a good response to imatinib. We
/ m* g5 {. F" y) r8 j' @$ ldescribe three patients with stable complete molecular response on dasatinib
; s: Q/ p8 s: B+ Q htreatment following imatinib failure. Two of the three patients remain in
1 Y% N7 B9 R& s6 Lcomplete molecular response more than 12 months after stopping dasatinib. In% I. O r: D4 F* D
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to. b9 _) @# u, g
show that the leukemic clone remains detectable, as we have previously shown in$ x5 c# Q# h9 z* H
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
3 q/ q" k9 y2 C; \the emergence of clonal T cell populations, were observed both in one patient
4 c; K! C& d5 i: b% [# h- h7 |who relapsed and in one patient in remission. Our results suggest that the
& o( k/ ?1 [4 Q: ^6 Wcharacteristics of complete molecular response on dasatinib treatment may be
% l/ o x' R6 m* W: |' @9 qsimilar to that achieved with imatinib, at least in patients with adverse8 a# O# t2 m; t: M9 W$ S. a- M
disease features.
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