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 B1 q' b1 q6 m; z- Z 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。& Q" s! \; L( U
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作者:来自澳大利亚0 S: S; h0 f- \3 c! d
来源:Haematologica. 2011.8.9.
: O9 v y! x t+ e. \Dear Group,
: z W5 ~4 Q% {3 J
& N* C, N2 g5 Z, oSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
) T) k9 T* r: ^3 H$ Y7 ~; Ytherapies. Here is a report from Australia on 3 patients who went off Sprycel4 b4 D% | ] m: P( A4 v) r' a
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 Y$ K/ q( |/ b- Z/ Sremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
! |3 u; `, L' Z' @' E7 Fdoes spike up the immune system so I hope more reports come out on this issue.. C, h: |* @4 a4 _! N! c- a
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The remarkable news about Sprycel cessation is that all 3 patients had failed% V3 I( h; m( _1 J, d
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
$ w4 y1 Y! w( z) F$ X9 rdifferent from the stopping Gleevec trial in France which only targets patients
% |& A( k1 ]8 Z+ c* t; |9 ~8 }- [4 zwho have done well on Gleevec.
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& [, ~& M" J; p5 q6 D. K' d1 bHopefully, the doctors will report on a larger study and long-term to see if the
6 ^# F1 v# q7 Z a B# fresponse off Sprycel is sustained.0 ~, Q& p4 c7 Q8 J& I) ?
# a9 o3 p" g$ M9 e" |- Q8 \6 pBest Wishes,
# l" b' [( C3 r* L. z$ C* XAnjana; F' l, k. l0 j- s
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Haematologica. 2011 Aug 9. [Epub ahead of print]2 W" j* H; d: b2 K* m) {6 p* [/ i" E
Durable complete molecular remission of chronic myeloid leukemia following
0 S2 ^& m0 {% |6 t: adasatinib cessation, despite adverse disease features.) e$ d6 n2 e Y% r/ z0 G
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP./ q) W! B# y. f! G% g- C* H
Source7 u$ B6 \4 }. e2 j
Adelaide, Australia;" j( t" k8 a9 W7 P$ R: ^' K7 r
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Abstract
g1 j0 a+ w5 u( \" g, i/ e! rPatients with chronic myeloid leukemia, treated with imatinib, who have a
$ T; M2 g% W; Edurable complete molecular response might remain in CMR after stopping( U5 t0 X' r5 f. P; S( }
treatment. Previous reports of patients stopping treatment in complete molecular
) O7 S; K' e8 i9 P; M6 ~' Tresponse have included only patients with a good response to imatinib. We* A* _0 d' J3 X
describe three patients with stable complete molecular response on dasatinib2 I+ X) n% G$ x4 R7 g, M( i& z6 U4 E
treatment following imatinib failure. Two of the three patients remain in, ~' `( @& s* h# U D' O4 P
complete molecular response more than 12 months after stopping dasatinib. In
2 x4 Z! p% A+ B4 Kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
- U# W0 \, q; o+ U# D/ mshow that the leukemic clone remains detectable, as we have previously shown in
) h5 d$ p- y9 y @5 R J/ l& gimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
7 e' [4 l5 a3 s" ~$ \8 H6 \the emergence of clonal T cell populations, were observed both in one patient: ?* H: P5 w8 s' L! a* O( o/ I; }) \& Y$ Z4 i
who relapsed and in one patient in remission. Our results suggest that the
5 g, Z" E! q: w, T6 s9 Kcharacteristics of complete molecular response on dasatinib treatment may be
4 _9 @( ~- v' C, v& isimilar to that achieved with imatinib, at least in patients with adverse
) N$ }) ?8 C9 S+ R7 s6 \) g5 kdisease features.
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