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。7 O- d, E! j, p5 U: U0 O* P- D+ W
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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& T3 H: H1 W: M6 Z作者:来自澳大利亚% K" R" ]7 t3 X" J B9 P+ A
来源:Haematologica. 2011.8.9.$ j6 z$ w. B( U t# L: E
Dear Group,5 P/ K4 A; B7 S) @9 Z
- @: |8 p! Y- `4 FSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML& v; I1 e) w8 g* B& J$ b
therapies. Here is a report from Australia on 3 patients who went off Sprycel
- A: y. l8 T% u9 g" a; I8 Nafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients+ r4 i V' d" y; r. y" Q
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. ]# B) p/ q, @2 z0 M4 s% Y6 R
does spike up the immune system so I hope more reports come out on this issue., k$ v) [4 I4 T% W% G% _
5 B! N+ H5 z& h: M& {
The remarkable news about Sprycel cessation is that all 3 patients had failed
. }7 r8 b3 w# |7 @. L9 nGleevec and Sprycel was their second TKI so they had resistant disease. This is
- ~" @. i, f0 Idifferent from the stopping Gleevec trial in France which only targets patients0 P$ t" \0 g/ X. T7 d; X
who have done well on Gleevec.6 k1 W8 b9 `- J* R- {, V4 I. u2 @
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Hopefully, the doctors will report on a larger study and long-term to see if the
9 s4 A' U6 R! |7 `/ x6 \0 [response off Sprycel is sustained.$ ~0 j3 V; M9 E2 j' L0 T
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Best Wishes,
% o3 \1 _% E) S2 mAnjana( q; }& P0 S" c, S6 f K4 e6 m
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5 \2 V( _3 @" k/ R5 J2 k( w3 dHaematologica. 2011 Aug 9. [Epub ahead of print]
5 C) J8 P( j% \$ b$ eDurable complete molecular remission of chronic myeloid leukemia following2 f8 {9 _0 {, r& s
dasatinib cessation, despite adverse disease features.6 |! x$ A' v- e' c
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.9 H' j; |8 h9 b" D5 v
Source
- N( w; S- ~. q$ X ?Adelaide, Australia;1 v, C' {. M/ ?' d1 F
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Abstract. Y& z5 _1 | f A* H9 ?( \
Patients with chronic myeloid leukemia, treated with imatinib, who have a: \$ A+ {+ z; ~/ e9 L g$ q
durable complete molecular response might remain in CMR after stopping' n* ]/ c$ v2 Y2 g; ], H2 ~
treatment. Previous reports of patients stopping treatment in complete molecular
( M2 H. z. R3 j1 _/ X m& Oresponse have included only patients with a good response to imatinib. We$ u W! G5 E; {$ c) y
describe three patients with stable complete molecular response on dasatinib
2 v( T. j! Q5 w" U7 Streatment following imatinib failure. Two of the three patients remain in( b, s# ^2 S+ d1 V
complete molecular response more than 12 months after stopping dasatinib. In
/ g% _- @0 u7 k3 T Q& C1 W6 y7 Kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to+ c' q6 d0 D4 r% X3 i: P$ F! H2 t' D; q
show that the leukemic clone remains detectable, as we have previously shown in
" X! T& S, W) rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as- C5 ], Q, c4 P
the emergence of clonal T cell populations, were observed both in one patient/ u7 `0 L; ]1 l8 {# D
who relapsed and in one patient in remission. Our results suggest that the+ ?9 Y8 w* ]$ g! s k" O, v
characteristics of complete molecular response on dasatinib treatment may be
6 m c# p6 G7 k0 f' Tsimilar to that achieved with imatinib, at least in patients with adverse7 q& ?, g( u9 V4 i! M; V
disease features.
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