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。
. Y) U5 R/ C/ M7 O 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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3 S" m. |$ j! s作者：来自澳大利亚, G! w8 _2 y- _6 A4 c+ x0 ]
来源：Haematologica. 2011.8.9.
3 P0 Q2 }$ T/ ~/ M$ a5 NDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML! H6 q& C- G0 Y$ t
therapies. Here is a report from Australia on 3 patients who went off Sprycel
9 _) K/ b7 j! V( O1 r X: Qafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients7 m5 \, L: d; v. h* J+ t
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
% }# m; i- }6 ^" ]" wdoes 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
$ ?! i* E' ~6 _: ~0 F5 NGleevec and Sprycel was their second TKI so they had resistant disease. This is7 G! f2 ?: X# r; O" `# }, m1 }
different from the stopping Gleevec trial in France which only targets patients
5 X8 z) G% S+ K: I1 V/ Xwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the4 l& k% f y- [" T; s; ]8 W8 x* J/ p3 L% o8 G
response off Sprycel is sustained.% Y. Z1 p+ l/ h' H' ]
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Best Wishes,
; L7 q/ t1 `5 r1 q& Q7 wAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]- k3 O, `6 O$ t9 R
Durable complete molecular remission of chronic myeloid leukemia following0 X0 D8 O7 `4 X! |4 ^
dasatinib cessation, despite adverse disease features.
; B; n9 B% B1 n `6 s! k+ P- T" kRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.8 p% |2 \7 m+ s" T |# U6 h' E' }
Source3 P8 b9 }0 N% W" _8 S" W" h. ^
Adelaide, Australia;4 O' Z/ E8 H- r) V. ]
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Abstract
9 C. W: M2 r1 N" U" mPatients with chronic myeloid leukemia, treated with imatinib, who have a0 c% O; k- V& r5 Q+ H) x8 f
durable complete molecular response might remain in CMR after stopping
3 L1 t. s5 q. K9 E0 [& j/ V! |! [5 ltreatment. Previous reports of patients stopping treatment in complete molecular
2 U/ w: Q+ n& [1 N; c1 X. Sresponse have included only patients with a good response to imatinib. We
7 n+ t. ]4 T5 s' o) d0 ^0 Zdescribe three patients with stable complete molecular response on dasatinib
2 n+ N4 p: R" I7 I. c8 wtreatment following imatinib failure. Two of the three patients remain in$ O' b6 R7 G& u6 e) G+ L# i% Z
complete molecular response more than 12 months after stopping dasatinib. In
3 c. q" {' P$ V1 l- a1 Z1 k% F) zthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
6 B8 r' e2 i: x% L2 Mshow that the leukemic clone remains detectable, as we have previously shown in7 o5 _1 p6 E# v+ Y
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
" ]3 G. f! m" f& L- W) d2 O7 W9 {the emergence of clonal T cell populations, were observed both in one patient
2 ~4 P8 y- N+ c5 n/ V* I7 \* fwho relapsed and in one patient in remission. Our results suggest that the
4 d& ~6 \+ G* A5 I* H' ^characteristics of complete molecular response on dasatinib treatment may be
3 D, e: E; I1 X3 g& Vsimilar to that achieved with imatinib, at least in patients with adverse* R$ _" X7 ~ _3 D0 k
disease features.
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