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。
# A8 Q8 h- P2 }! F- V( L5 O' J, } 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
6 I" X# ], U/ d9 v* V( [. }来源:Haematologica. 2011.8.9.
, r. [. Z9 B9 K3 CDear Group,
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$ a5 A$ B& ]7 M* JSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
$ o* B Q) i3 F7 V( G/ i+ Ctherapies. Here is a report from Australia on 3 patients who went off Sprycel, j' l$ A3 i8 ^% @2 s
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
1 Y5 m) k8 z9 K: L- \7 uremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
7 b& `( h* Y- A1 E3 [does spike up the immune system so I hope more reports come out on this issue.) R& R) H$ d3 r- F/ Z
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The remarkable news about Sprycel cessation is that all 3 patients had failed% ? K. l9 e9 F8 P5 {
Gleevec and Sprycel was their second TKI so they had resistant disease. This is! [+ U I" z2 A7 P5 j
different from the stopping Gleevec trial in France which only targets patients. E7 w/ f2 m. F7 `( G$ Q
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
7 ^9 [; K ?0 Wresponse off Sprycel is sustained.( h4 L! N( o0 ~
" u7 j b9 e1 LBest Wishes,
( \3 O) d( I' J0 UAnjana$ e6 ?. i& V/ T1 J/ n9 ~8 u9 C! P
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* d$ U( L0 C8 g, @; {9 h: dHaematologica. 2011 Aug 9. [Epub ahead of print]
7 J4 r6 u9 r" r8 m" y; }. MDurable complete molecular remission of chronic myeloid leukemia following
p5 ?) z2 z$ J; y# ndasatinib cessation, despite adverse disease features.
1 u# M L, i/ Q& @* kRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
& ?1 K; C$ C4 z' `1 `; KSource
& h& ^- ]0 O3 J3 b5 gAdelaide, Australia;
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# l; r6 o* D9 g# ~& W3 s! @Abstract
( a" T, [; j8 N! l" YPatients with chronic myeloid leukemia, treated with imatinib, who have a
) _% u& I6 U- s6 F3 K7 ^7 Idurable complete molecular response might remain in CMR after stopping( b/ S3 F7 y. W( P% E
treatment. Previous reports of patients stopping treatment in complete molecular
/ q; O$ x& a0 ?4 k( Dresponse have included only patients with a good response to imatinib. We5 I: L# d l% d" S& S1 m/ e
describe three patients with stable complete molecular response on dasatinib" U8 y) O5 z2 s1 V' ?9 \$ y
treatment following imatinib failure. Two of the three patients remain in
, S g: g# t' ^5 c" k3 `complete molecular response more than 12 months after stopping dasatinib. In
7 g; Y) Z& u- M6 D( `/ jthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
5 c- p: G1 l6 S# x0 fshow that the leukemic clone remains detectable, as we have previously shown in
/ F8 R- o1 b/ j/ I1 a; Pimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
/ s5 e% h0 ]4 o( \9 a* G ~the emergence of clonal T cell populations, were observed both in one patient/ {* |2 ~# e& }8 g" @- x8 |: y$ W
who relapsed and in one patient in remission. Our results suggest that the" b3 M' x0 l7 A! D7 @/ t2 o
characteristics of complete molecular response on dasatinib treatment may be
* `+ X* t/ H6 _# P2 h+ nsimilar to that achieved with imatinib, at least in patients with adverse- v- t+ _1 a6 T) i. J/ g0 v, A
disease features.
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