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。
I6 ?9 B! s8 S; @% E' H7 v5 N 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。" A9 @) h- P8 F8 O6 Y
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作者:来自澳大利亚
5 ^. e7 u" f4 N8 I$ X8 s* `0 [+ G来源:Haematologica. 2011.8.9.
1 Y; B3 S* m6 l- fDear Group,( C0 C% q8 o8 N1 o
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML, g6 ^6 g& J! B# f- X4 Q) r
therapies. Here is a report from Australia on 3 patients who went off Sprycel5 n: C7 X2 r# [$ H
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients$ d$ N; s6 A0 u
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel3 L7 F! |' W3 F8 }! \+ J
does spike up the immune system so I hope more reports come out on this issue.
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$ x2 M$ Q& c$ H1 o1 VThe remarkable news about Sprycel cessation is that all 3 patients had failed
9 f, b) o1 R: ^3 ]Gleevec and Sprycel was their second TKI so they had resistant disease. This is
: e: k, `7 m) y2 C2 X4 i K6 Fdifferent from the stopping Gleevec trial in France which only targets patients
+ G* ~8 ]4 p* c4 zwho 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
$ d1 S5 @$ c9 R, i6 O, h" Presponse off Sprycel is sustained.
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( @8 w3 D }3 j: t/ QBest Wishes,$ T- K8 Q4 W( f. a
Anjana9 F: l2 I. Y4 U ~6 G# ?) ?( U$ c1 f
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Haematologica. 2011 Aug 9. [Epub ahead of print]
, y( }9 U: A# p2 P4 rDurable complete molecular remission of chronic myeloid leukemia following3 ?: [+ l) i* f7 J. A' U* H
dasatinib cessation, despite adverse disease features.5 v2 K( _7 x+ u0 h. |
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
* S4 r- F1 A5 r2 t% m" k" K) FSource# ]& g) r! i& i" O$ z. X9 l
Adelaide, Australia;
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Abstract( e E& j/ W( X, ]! g
Patients with chronic myeloid leukemia, treated with imatinib, who have a
* a4 F* R* g# p2 t7 k3 C, adurable complete molecular response might remain in CMR after stopping
+ M, b. p W6 Wtreatment. Previous reports of patients stopping treatment in complete molecular' n' f. p2 c& Y5 c5 V3 `9 o, i9 j2 I4 a
response have included only patients with a good response to imatinib. We
4 z9 `/ U, v8 r2 {describe three patients with stable complete molecular response on dasatinib( f) j2 ]& W$ A2 x s+ J
treatment following imatinib failure. Two of the three patients remain in
2 e$ Y8 ]' n+ @3 p @complete molecular response more than 12 months after stopping dasatinib. In% F3 _0 K6 T4 }: U+ j% b
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
$ f$ r) U5 R& }. z( T5 Bshow that the leukemic clone remains detectable, as we have previously shown in( S( k% } i6 R; v! Q( d5 K6 J
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as0 E q* h- |5 t8 ?
the emergence of clonal T cell populations, were observed both in one patient) o' A8 D5 k% g. n9 n& s: M+ Y/ Z9 ?+ ?
who relapsed and in one patient in remission. Our results suggest that the
1 |3 u# w3 f7 S& ^" d0 i- N% O# f# dcharacteristics of complete molecular response on dasatinib treatment may be* {( e' _ q3 t( H
similar to that achieved with imatinib, at least in patients with adverse
1 a0 P9 z4 X \( F( Fdisease features.
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