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。' g/ F' Y! {* q, B% s& N$ c; E
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; A4 @9 B9 L& I- o# x) ]. K
来源:Haematologica. 2011.8.9.
% e( w+ X0 g- n+ v v9 a$ C! pDear Group,
- \+ t# A( @* Q$ g4 d" y
$ q- i" ?( Z; u7 x1 k, D: ?9 u" USome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
1 O8 L+ `3 s: K( h( Q% N2 K! Gtherapies. Here is a report from Australia on 3 patients who went off Sprycel: ~3 U9 Q* K+ h M& i( ~0 N
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
7 T! Z( r/ k9 Z6 C: P$ lremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel6 k+ _0 r8 {1 {/ O5 J
does spike up the immune system so I hope more reports come out on this issue.
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- P8 q" P! P, P6 J. |, l) ~& @! gThe remarkable news about Sprycel cessation is that all 3 patients had failed. S% h$ d+ ?! q* _. U- o
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
( ?/ J3 n* U9 O$ X0 I0 \% ^different from the stopping Gleevec trial in France which only targets patients
+ i. g( _& ], v8 f& ywho have done well on Gleevec.
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* U, B: Z& T" ^# l1 zHopefully, the doctors will report on a larger study and long-term to see if the
( h6 O7 j7 z$ i2 l4 tresponse off Sprycel is sustained.5 d# v9 [% J3 s# j% n( v7 D" \/ |
' n5 R$ a: n$ P3 aBest Wishes,' n0 \$ a% u/ @; j& w# l6 p( m
Anjana5 D6 ~' S0 ?/ r0 S; S6 O( u
z" D2 J' g% d$ ?. ^
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# O- k( n- p5 l: d4 P; aHaematologica. 2011 Aug 9. [Epub ahead of print]2 ?' ~8 }& H. H1 E4 q8 K) o
Durable complete molecular remission of chronic myeloid leukemia following
5 l N. J8 y# ~ o* H6 d9 G- A. wdasatinib cessation, despite adverse disease features.
5 y* X W M: ^& @- G% SRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.- Q: f2 p3 S0 H R
Source
8 o }; \9 _ R" q+ K& J' S- h0 JAdelaide, Australia;
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Abstract
0 Q; S9 M. p; f5 UPatients with chronic myeloid leukemia, treated with imatinib, who have a
* ^. F6 A, J/ Z/ ]durable complete molecular response might remain in CMR after stopping3 t3 \/ C6 u! J2 W, c% a% x
treatment. Previous reports of patients stopping treatment in complete molecular
7 l3 l9 a" s; D6 wresponse have included only patients with a good response to imatinib. We9 C! ^3 ~" L: {7 c% H3 @ H
describe three patients with stable complete molecular response on dasatinib
+ M+ B) `8 m' ]* ^4 v2 a1 x6 b3 S' Y; Mtreatment following imatinib failure. Two of the three patients remain in$ ?- t2 ?( y( i% t7 G
complete molecular response more than 12 months after stopping dasatinib. In
' D* {. t% e# P3 Z6 kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
8 W1 ~9 D- q1 R) ?show that the leukemic clone remains detectable, as we have previously shown in5 B+ l4 V! G5 o' I
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
0 N6 ?1 \( w* m; D& Z6 E& K5 kthe emergence of clonal T cell populations, were observed both in one patient
! ]2 T9 t* `- {6 ]* v, H7 f, kwho relapsed and in one patient in remission. Our results suggest that the) u+ I3 y8 X* ^ u h/ i
characteristics of complete molecular response on dasatinib treatment may be
% |0 ^, e% g6 `$ g" _# zsimilar to that achieved with imatinib, at least in patients with adverse2 Q- z& e; j( O7 ^) ]
disease features.
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