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。1 i' K) \) \% v! x6 c4 S) |* a
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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作者:来自澳大利亚; T" f5 {: l8 z
来源:Haematologica. 2011.8.9.- A4 V* |- `3 R. V+ v
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML( y# [5 L2 j0 v1 [. g8 ?
therapies. Here is a report from Australia on 3 patients who went off Sprycel
, d9 X2 u/ a* u0 U7 `- cafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
3 T& n7 q$ w) `) A" \! K- ]remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel* g2 }/ Y. _* g/ X1 u% |
does spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed
0 |2 Q* |4 m- Y5 o. g8 ]# NGleevec and Sprycel was their second TKI so they had resistant disease. This is
6 e5 M: r& m# u: U; S, Jdifferent from the stopping Gleevec trial in France which only targets patients6 E! k+ Q3 w9 A1 V
who have done well on Gleevec.! b/ _) q+ y0 r. {) a6 r6 K
! ~/ q7 p9 O+ Q: G' e1 THopefully, the doctors will report on a larger study and long-term to see if the2 Y+ r/ a6 ]4 b+ _2 A E
response off Sprycel is sustained.
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: X+ l m/ g; rBest Wishes,
3 J% g( O4 e, J9 K& l+ n& z/ `Anjana, I W& B/ z2 n3 A# E
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Haematologica. 2011 Aug 9. [Epub ahead of print]/ M0 k8 `* L$ Q7 z
Durable complete molecular remission of chronic myeloid leukemia following, p9 Y, e k+ g
dasatinib cessation, despite adverse disease features.
6 B" g/ u- v0 t# CRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( R, z2 b+ f- L6 m
Source0 @" S; Y7 K3 \/ O+ a! y3 E
Adelaide, Australia;; O0 W7 M' Y/ z1 T; S
]- |/ c: w$ |: x; rAbstract1 \; W5 |1 R- J
Patients with chronic myeloid leukemia, treated with imatinib, who have a
; ^ y- C7 Z, |durable complete molecular response might remain in CMR after stopping4 l; D; e0 ]; i
treatment. Previous reports of patients stopping treatment in complete molecular
$ K% J, Q9 O. T( M7 T+ Presponse have included only patients with a good response to imatinib. We
9 q) ]+ }% [- s/ E |' w" u# F" Xdescribe three patients with stable complete molecular response on dasatinib
' J; I% y& ]& W R6 t6 D ztreatment following imatinib failure. Two of the three patients remain in
{ N$ j' `; { F. Ucomplete molecular response more than 12 months after stopping dasatinib. In+ P% T0 e6 b8 ^. D }1 |& w% k
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to- i$ Y$ U h6 O& r T7 t" }: r: M
show that the leukemic clone remains detectable, as we have previously shown in
/ G. v! B9 q0 O0 u4 Q0 B4 Yimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
3 e& }% j' z) @- D( wthe emergence of clonal T cell populations, were observed both in one patient
' B0 T; X; P2 D5 M% H$ D1 Rwho relapsed and in one patient in remission. Our results suggest that the" [" M; U% t$ d& o7 O
characteristics of complete molecular response on dasatinib treatment may be, V, e& P( V- I
similar to that achieved with imatinib, at least in patients with adverse
' V4 h# z, p( X% W4 ]disease features.
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