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。+ F2 c0 O. |. @+ Q 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。$ V0 T5 N, K }5 f) u5 p. {
0 m) P& p3 Y7 \! n; T作者:来自澳大利亚8 Z$ G: L& D0 T9 f; o
来源:Haematologica. 2011.8.9.; M6 h( H ?! B H
Dear Group,6 L& `' A1 T/ e, h1 X8 C0 r
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML. F* h2 f c/ {+ l; _+ `
therapies. Here is a report from Australia on 3 patients who went off Sprycel
" U- y3 U! L1 b; ~. {0 hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients3 }# h* S2 l1 s6 B R: j
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel0 F: d |1 H: ^ N; [
does spike up the immune system so I hope more reports come out on this issue.
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$ d5 v' z# P' e- v0 uThe remarkable news about Sprycel cessation is that all 3 patients had failed
! E( W m+ R, E1 E/ Z' R! d% eGleevec and Sprycel was their second TKI so they had resistant disease. This is
' |1 l) {4 q/ G; z. C+ W6 P4 U3 K# xdifferent from the stopping Gleevec trial in France which only targets patients9 N1 t' w4 _9 P# F
who have done well on Gleevec.
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" N" A. x) G) j7 sHopefully, the doctors will report on a larger study and long-term to see if the, t9 G% ?8 c* C/ o& X+ f. L! H; H
response off Sprycel is sustained.
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( n4 @" Y: ^+ b% t D$ PBest Wishes,' J9 G7 i9 s, ^+ e5 q4 W U# n
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
2 k$ s1 O: _& T% M+ SDurable complete molecular remission of chronic myeloid leukemia following7 l* {3 K1 R$ e1 k$ U. V4 D0 D8 C; H( Z
dasatinib cessation, despite adverse disease features.
, x# o8 X5 x# p! }Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.& I/ D! p% ^; D8 `
Source
" V Z$ j" Z. \: R( g( ]Adelaide, Australia;' [$ g$ f; k0 Z8 q
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Abstract
, ^5 M* d' Q+ w3 ^Patients with chronic myeloid leukemia, treated with imatinib, who have a
& |; J8 s+ U! @$ u4 ^) _durable complete molecular response might remain in CMR after stopping: H& a* Y V2 I+ ?0 C& [$ F/ D$ g5 J
treatment. Previous reports of patients stopping treatment in complete molecular
3 C9 x$ X+ t2 F1 Yresponse have included only patients with a good response to imatinib. We
! A" ~& e" g& i% f2 u% C( e3 kdescribe three patients with stable complete molecular response on dasatinib
/ {+ k4 C/ p) D r8 Xtreatment following imatinib failure. Two of the three patients remain in
' X# ~' C) K- ~7 I Ecomplete molecular response more than 12 months after stopping dasatinib. In8 k. m; f+ N. a h) L1 ?: a
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to5 z3 Q$ Z/ ?6 |' Q9 R, F0 {
show that the leukemic clone remains detectable, as we have previously shown in4 |# |+ d1 C' y, i' h
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
( C, b" a, j3 k- c& p: bthe emergence of clonal T cell populations, were observed both in one patient* j. c: Q. h: A+ G
who relapsed and in one patient in remission. Our results suggest that the
2 \% J# {" h& f# ?; ]characteristics of complete molecular response on dasatinib treatment may be; o: D* y5 a I- ^
similar to that achieved with imatinib, at least in patients with adverse
+ d/ l' x4 V2 a: v; Edisease features.
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