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。. ~' D2 h3 e9 E6 U# o0 {
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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. r' M# U9 p( X- V3 I作者:来自澳大利亚
0 i( f6 A" x# E$ b! I, a1 F来源:Haematologica. 2011.8.9.7 u# j4 S' n# L( L; F! C9 L8 c
Dear Group,) v) `" V, K6 s6 O4 I6 y
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
# S8 @3 {- p, G- [ Z: \: P0 Rtherapies. Here is a report from Australia on 3 patients who went off Sprycel% Q" G L$ t$ L) r5 P0 }
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
A% Q) ^7 L3 V `remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel# h" R8 Q& n, f0 y5 ^
does spike up the immune system so I hope more reports come out on this issue.
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+ X* [7 y3 P' g6 wThe remarkable news about Sprycel cessation is that all 3 patients had failed
% K6 |4 n7 `4 l+ eGleevec and Sprycel was their second TKI so they had resistant disease. This is) S! e. q- g( U( Z& Z& a+ Q) r
different from the stopping Gleevec trial in France which only targets patients
" |" E$ I2 q5 s/ b7 i2 u1 o4 fwho have done well on Gleevec.
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3 Q# X, M# v- r! J$ y/ p! X$ H) r/ RHopefully, the doctors will report on a larger study and long-term to see if the
1 g3 n! _/ l" y9 f# Bresponse off Sprycel is sustained.
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Best Wishes,/ c( p5 G& k1 {. p' y8 ^* d% W% m
Anjana
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1 p3 H7 ], f) `7 |Haematologica. 2011 Aug 9. [Epub ahead of print]/ q" i) n. C' k, [
Durable complete molecular remission of chronic myeloid leukemia following. h4 b7 \7 f2 v r5 s* _
dasatinib cessation, despite adverse disease features.9 f5 D0 G' x7 d
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
- J. V' A+ P- a7 i5 {. K" LSource
5 F( Z6 y5 V1 x# Y3 m- ZAdelaide, Australia;& |! R b* C+ J6 x) N G
/ m* L' O2 F" t4 iAbstract
7 A) Z' I6 |, M# ?Patients with chronic myeloid leukemia, treated with imatinib, who have a
+ p' f3 i- V( ^: U8 k; Mdurable complete molecular response might remain in CMR after stopping
3 S" R- f4 P) G4 N4 Rtreatment. Previous reports of patients stopping treatment in complete molecular8 G0 ~8 I ]1 q+ s$ h
response have included only patients with a good response to imatinib. We
2 z; g7 c7 k; E+ C: s wdescribe three patients with stable complete molecular response on dasatinib
) z' g9 Z5 [ Y! v0 W3 H# Utreatment following imatinib failure. Two of the three patients remain in
9 V; ?) P8 ^7 ]& ^7 z9 l% `complete molecular response more than 12 months after stopping dasatinib. In2 F: R( Y9 _: q! |3 @4 Y
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to$ `4 Q7 C, t: f) z4 k8 Y
show that the leukemic clone remains detectable, as we have previously shown in
& q1 `3 U, M3 `: d7 u* T& qimatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 |# [8 e; T/ |6 a% U9 c
the emergence of clonal T cell populations, were observed both in one patient3 j% F/ A+ S) F$ H
who relapsed and in one patient in remission. Our results suggest that the
0 ^+ t* ?$ Q7 O' icharacteristics of complete molecular response on dasatinib treatment may be. V; Z8 P8 W. A4 F& }* g
similar to that achieved with imatinib, at least in patients with adverse
' H" Y& x) c* ~7 N! A& ^( {3 S6 L ddisease features. V2 z! Y" O% w3 l+ {1 Y
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