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。
6 B% {! x* F/ I5 g5 }: v% J$ Q: ] 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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0 W0 S+ _2 D6 S作者:来自澳大利亚+ n0 t! c: d5 n- W l0 `" U) D
来源:Haematologica. 2011.8.9.0 z p+ m# s& q
Dear Group,
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: F7 _6 Y ~. e5 E( TSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, z1 O: L" ^) S9 ]( s* f) w4 |therapies. Here is a report from Australia on 3 patients who went off Sprycel
+ Z7 q& s; e6 q; }after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
o/ G% }6 R. P: T. Y5 Cremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 k! B. N: H7 Q" k3 L& E" {! x
does spike up the immune system so I hope more reports come out on this issue.$ i3 D: f6 m% @8 O8 j1 S
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The remarkable news about Sprycel cessation is that all 3 patients had failed
' l d. r0 l6 [/ OGleevec and Sprycel was their second TKI so they had resistant disease. This is. g8 F& o7 [' ^! ^5 r
different from the stopping Gleevec trial in France which only targets patients2 n$ |& k ^1 G: J# [
who 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
' ?9 v+ g+ V7 J- P! b& Y. ?response off Sprycel is sustained.
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Best Wishes,0 _( ~3 ^& ]4 L+ `4 o% e
Anjana
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7 q$ C3 q5 u3 G+ n+ u. V0 w% oHaematologica. 2011 Aug 9. [Epub ahead of print]& C+ I0 B7 ^' X$ _1 R
Durable complete molecular remission of chronic myeloid leukemia following
! Z- S6 L5 }" d2 F: ndasatinib cessation, despite adverse disease features.
* s0 B7 |' O% G7 URoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;# |8 h6 p" o0 n( a& x
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Abstract
% E( R/ K V( R3 |% P1 x2 cPatients with chronic myeloid leukemia, treated with imatinib, who have a
$ ?+ J# M0 [5 M# m& C5 g% t& [. Gdurable complete molecular response might remain in CMR after stopping
4 O& L9 m7 @8 G G5 t& G5 \treatment. Previous reports of patients stopping treatment in complete molecular6 R8 c, X$ l1 S; K7 t7 Z
response have included only patients with a good response to imatinib. We
% m3 A. [& _. k3 @4 Mdescribe three patients with stable complete molecular response on dasatinib
! Z* N e" L' P: D- L; V9 Streatment following imatinib failure. Two of the three patients remain in% O# n) R% q- s; C8 R( l: y3 O
complete molecular response more than 12 months after stopping dasatinib. In, l- r X' m+ W9 ~
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to0 d3 H. F$ i; Q5 |
show that the leukemic clone remains detectable, as we have previously shown in7 ]+ i" @6 j. b# D
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as6 ~8 ^! G! [ k% @) {" i/ \) Z
the emergence of clonal T cell populations, were observed both in one patient
5 x7 r* N- L, C. h2 Uwho relapsed and in one patient in remission. Our results suggest that the* H/ p; z" r% b6 P
characteristics of complete molecular response on dasatinib treatment may be
1 C7 H, E! E+ g3 g+ n7 v! q1 Qsimilar to that achieved with imatinib, at least in patients with adverse q w6 L: K: [ @3 X( V
disease features.
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