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。
7 Z$ ~# @6 `5 l 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。4 ^5 b; c+ j# T% s; I- p
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作者:来自澳大利亚% \% R: c3 k: N* N; s* c9 ]% L% Z
来源:Haematologica. 2011.8.9.% E) h' v+ h2 b4 M: X
Dear Group,; |" K9 o+ U. {% b4 @) h) b
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
/ @9 F2 T, j' A: c0 G* ktherapies. Here is a report from Australia on 3 patients who went off Sprycel
. Z: Q* o; I9 Mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients# n3 D) U) N% K& e! G
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 k8 z8 o9 ~% r, B9 p
does spike up the immune system so I hope more reports come out on this issue.
' A/ n6 L m3 ], m0 P3 D6 S& l) O
The remarkable news about Sprycel cessation is that all 3 patients had failed& ^ U8 |5 y" m$ Y0 N) D
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
8 V# h7 @& J1 f! Q3 |$ Sdifferent from the stopping Gleevec trial in France which only targets patients' k# a$ `3 R; |& ~
who have done well on Gleevec.
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1 |8 g+ {8 i' q% l$ W+ \# EHopefully, the doctors will report on a larger study and long-term to see if the
. K5 c* _; u' g j" g- f9 ~, e! presponse off Sprycel is sustained.
m( a: Q# S, _% t' T; @% s% m% u) z9 a1 M
Best Wishes,
8 A `! R0 O5 {) UAnjana6 t! U+ C1 F+ p1 n! H, t, a
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Haematologica. 2011 Aug 9. [Epub ahead of print]+ `. @, T. ]- X) D* b" P
Durable complete molecular remission of chronic myeloid leukemia following
0 Y5 H) e5 H( pdasatinib cessation, despite adverse disease features.
: O0 S1 O" a4 Q( V& _Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;
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3 K+ b0 w2 p( Z) |) ~+ J2 y' ]Abstract
# D5 x" A8 F; g) H) F8 i" ^5 WPatients with chronic myeloid leukemia, treated with imatinib, who have a, G" m I) W, Y$ V: D
durable complete molecular response might remain in CMR after stopping
+ M8 J C4 C) S0 Utreatment. Previous reports of patients stopping treatment in complete molecular- w7 F2 f- I+ n- N% F: X' F/ W2 O
response have included only patients with a good response to imatinib. We
# Y" _( a/ ]2 Y! m, edescribe three patients with stable complete molecular response on dasatinib- _: c X3 J. W/ i* @0 l
treatment following imatinib failure. Two of the three patients remain in
. O9 F( Z* p1 u& X2 Bcomplete molecular response more than 12 months after stopping dasatinib. In
; P4 u7 P1 w0 }, r1 M' `- Uthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
- K, v$ t' r. V+ {* Eshow that the leukemic clone remains detectable, as we have previously shown in2 k' T& ?9 p/ w0 s
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
3 b% z; y& [* |) y3 V& O! Ithe emergence of clonal T cell populations, were observed both in one patient) Y6 _: j1 p M c7 r, ^! C" i6 {6 A
who relapsed and in one patient in remission. Our results suggest that the
2 t' \9 Z. |0 N& X' qcharacteristics of complete molecular response on dasatinib treatment may be
; ~3 b- `0 M, x2 csimilar to that achieved with imatinib, at least in patients with adverse4 g' l7 u+ u/ C, N% c6 e
disease features.' A/ \4 R0 P% ]+ \/ r3 C
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