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。, H* N; d2 l- d3 \5 W+ G4 v; H' p
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。9 ?) q1 \, q2 X: `0 E$ v0 q
# l& B8 a6 h4 N# u8 o1 }6 ~, h作者:来自澳大利亚
0 }3 k4 S, m" `: E/ N1 ^& p* P来源:Haematologica. 2011.8.9.+ I) |" V( A T; E* _
Dear Group,
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8 X: j5 R$ u5 M) c7 V; G* I% p2 w, DSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML; s" g/ u, N/ U9 ^4 L
therapies. Here is a report from Australia on 3 patients who went off Sprycel
1 e* @7 _( E5 c# F& F- uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients+ U, @0 T4 B% Q" [9 d% R) F I
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel$ o7 ` h9 r0 V5 b* l8 e( M% F
does spike up the immune system so I hope more reports come out on this issue." f# @* t+ y' u( y7 X0 p! U
; U( W, Y# p. }5 a' OThe remarkable news about Sprycel cessation is that all 3 patients had failed
8 k% C5 @. @2 lGleevec and Sprycel was their second TKI so they had resistant disease. This is
& A# x, m) e$ c2 Qdifferent from the stopping Gleevec trial in France which only targets patients
5 B* w# G% Y) n/ Fwho have done well on Gleevec.
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' S8 S! H+ w' k- W6 f5 r8 G/ }Hopefully, the doctors will report on a larger study and long-term to see if the1 G0 ]5 `" N: F5 K
response off Sprycel is sustained.2 x5 D' o1 w/ V
# b5 o Z8 ~: e" [3 f6 }5 TBest Wishes,4 h! X9 W1 @* c& Y( m9 U$ \2 A8 R
Anjana2 A. c8 H1 `# V( g8 F- D) ]2 B9 X
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Haematologica. 2011 Aug 9. [Epub ahead of print]
8 L5 G6 n8 [3 h0 R5 WDurable complete molecular remission of chronic myeloid leukemia following
) C: j$ c6 e0 hdasatinib cessation, despite adverse disease features." [0 V' U; Z& a6 J
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
2 c( {7 l( E& n7 LSource' G% @: V G# B/ V9 ~
Adelaide, Australia;5 `! w+ d" Q; h* t% k! ^7 ~
; \, j9 c# ]4 j6 iAbstract
7 `- s( \+ f& Y/ a# T* z3 wPatients with chronic myeloid leukemia, treated with imatinib, who have a
+ s% D9 T4 K, c8 p7 e# z( ?6 N, Ydurable complete molecular response might remain in CMR after stopping9 R; X% G7 z4 a9 }0 F$ M4 g
treatment. Previous reports of patients stopping treatment in complete molecular4 Y$ j& r0 ~( ~5 ]/ ~7 m9 U
response have included only patients with a good response to imatinib. We
% `5 Z8 S/ F, [: fdescribe three patients with stable complete molecular response on dasatinib0 _% f Q- }5 T+ Q3 t4 _' r0 Q
treatment following imatinib failure. Two of the three patients remain in5 C: K$ c! u9 h6 }
complete molecular response more than 12 months after stopping dasatinib. In1 y) U* @2 [6 |7 D1 s8 b) B. E
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to+ g' ~" ^3 a: s: D
show that the leukemic clone remains detectable, as we have previously shown in
$ n; }; i/ [/ S$ Timatinib-treated patients. Dasatinib-associated immunological phenomena, such as
{- H# J# P9 T0 v6 X" Lthe emergence of clonal T cell populations, were observed both in one patient
: i* g, W- h Y) Fwho relapsed and in one patient in remission. Our results suggest that the) x8 A A- _& Q; _
characteristics of complete molecular response on dasatinib treatment may be
; L9 B" |! b5 `. {. ksimilar to that achieved with imatinib, at least in patients with adverse# q. o9 N& w5 `( k% \2 f8 ]& g
disease features.
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