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。
3 q! w* o3 s! b( v& Z3 U% d& @ 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2 l# Q: d' n! q5 I! d
来源：Haematologica. 2011.8.9.
4 h. I) ?4 R. C$ C6 h3 X N, o3 [Dear Group,
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7 v( G4 P6 p0 ]* Y6 {& s# i0 eSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 A. W% ~8 s, m! W% B/ H; m9 B
therapies. Here is a report from Australia on 3 patients who went off Sprycel
8 Z/ v8 \% P9 @0 uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients3 o: A' B1 G0 g x' ~5 i$ ^( A
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
$ N+ Y3 B7 Z% q6 g: t* Y: O9 q3 Bdoes spike up the immune system so I hope more reports come out on this issue.' i, x' @7 L$ \8 r6 A; P3 M
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The remarkable news about Sprycel cessation is that all 3 patients had failed- {+ Y# {' \, |5 M- D" a8 K
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
( l, o5 M0 ~; g; Y, \, _different from the stopping Gleevec trial in France which only targets patients
% h! }5 W: l0 t, T* T4 o2 |who have done well on Gleevec., u/ [- }/ S2 ^
& V. U. k5 N6 @9 i! r( rHopefully, the doctors will report on a larger study and long-term to see if the- i: f; `6 K* u6 C8 c# k8 w1 b: ^
response off Sprycel is sustained.6 D6 U% i& g; [& [
/ `( Z9 |& x. O TBest Wishes,. E- f$ S" q, B( _: Y: }
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]* B! @ D# Q7 O( W) _/ [
Durable complete molecular remission of chronic myeloid leukemia following
) C) U D. R; R; _( u% Qdasatinib cessation, despite adverse disease features.+ Z9 }; @+ H4 F8 {/ F3 h' ?, `
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
8 I* E3 x3 v. [6 ` @, vSource
2 ^3 J0 \7 T# Z5 y, ~ L! ~1 h& g5 F$ uAdelaide, Australia;
6 Q- f$ D2 M7 z- J( w1 w2 ^+ T+ f+ F/ w# G5 G
Abstract
+ N' i! f' z$ x- }Patients with chronic myeloid leukemia, treated with imatinib, who have a3 x% b# T5 p7 Q9 R# b+ l2 u8 v
durable complete molecular response might remain in CMR after stopping5 ?# F: {$ G) Q, W
treatment. Previous reports of patients stopping treatment in complete molecular
& q! G; u+ y w5 o5 N0 mresponse have included only patients with a good response to imatinib. We$ q" M6 Y7 N* K$ x0 w- y& {+ `" z
describe three patients with stable complete molecular response on dasatinib
, i ^! H( A$ h; K A, }) Otreatment following imatinib failure. Two of the three patients remain in3 ?# D6 a, o3 e. U0 C
complete molecular response more than 12 months after stopping dasatinib. In+ w3 ]2 M- c# j3 {* S9 [
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
/ V% C6 F" ~; _/ _1 |show that the leukemic clone remains detectable, as we have previously shown in* W, V' P8 ?) Y4 C! y# Z3 M; C5 P
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
% y4 }2 _+ ]8 ?; cthe emergence of clonal T cell populations, were observed both in one patient
; Q/ U2 B" o6 ?: Wwho relapsed and in one patient in remission. Our results suggest that the
# Y a, @# ?$ B7 T# y" scharacteristics of complete molecular response on dasatinib treatment may be
. o1 w6 D; m, B8 [! hsimilar to that achieved with imatinib, at least in patients with adverse" Y1 Z; b3 \2 c2 q! }: F: [4 N& q% W
disease features.
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