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。4 n, e% U% x- N+ D. L" x
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
0 x; o4 V5 x9 { N来源:Haematologica. 2011.8.9., C/ |& p! J4 K$ F" t) d
Dear Group,: U4 l" T/ e; G* K! H0 ~% x8 d
( Q& y. U, b- g+ b3 }Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
! p W5 u% ^9 ttherapies. Here is a report from Australia on 3 patients who went off Sprycel
, T8 _! s+ E9 W7 n7 L/ _6 @5 o: Cafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients1 X' n& s. } d( V
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel! Q$ G, t6 E% Z3 i! `
does spike up the immune system so I hope more reports come out on this issue.6 f- r+ p8 G+ R
1 G# I9 s8 w% y: A- a& GThe remarkable news about Sprycel cessation is that all 3 patients had failed9 N" ?& I, K8 |1 T- v- H2 Y
Gleevec and Sprycel was their second TKI so they had resistant disease. This is' z1 u: {2 _6 c& H' e- G0 T
different from the stopping Gleevec trial in France which only targets patients
% ]. U+ P$ h* V) S" R7 I. R/ kwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the* Z; ?% G" w0 Z8 t: q" {; q# v
response off Sprycel is sustained.
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Best Wishes,& }! M! H0 c: i' x
Anjana
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1 g( D0 ]( {+ j$ ?/ ` E, _Haematologica. 2011 Aug 9. [Epub ahead of print]1 u4 Y; O. l7 g
Durable complete molecular remission of chronic myeloid leukemia following
, F6 m, o/ R+ w6 o) P5 L) ?! }dasatinib cessation, despite adverse disease features.6 r2 t7 i! y( G0 ~0 Y+ C# D4 _ h
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
+ b, }: k8 I* R' U- nSource
+ l5 Y* A# z2 ?Adelaide, Australia;0 F% o( x: L$ i- w$ ~- j1 o
) p2 }9 b B7 q, _0 `+ {Abstract
1 F& u! j2 a* f$ C% t& w2 ~, _Patients with chronic myeloid leukemia, treated with imatinib, who have a' b D% o( {% F! ]
durable complete molecular response might remain in CMR after stopping
8 H% j; w; a/ ^- i/ A5 {/ a: jtreatment. Previous reports of patients stopping treatment in complete molecular2 g: q$ a$ f# _# Z
response have included only patients with a good response to imatinib. We0 ~ j$ g8 P0 ]& P
describe three patients with stable complete molecular response on dasatinib
2 @) N6 }- h; l( V% p z9 _% M- ytreatment following imatinib failure. Two of the three patients remain in
* A% i5 B" e8 ?- scomplete molecular response more than 12 months after stopping dasatinib. In
6 Q9 a9 c! T3 n; |" F) ~; ^these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to4 F! U; {1 W7 b+ D) Z
show that the leukemic clone remains detectable, as we have previously shown in, g9 w7 \' `8 J) O ?
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
- D6 @0 v2 ?' [! ?the emergence of clonal T cell populations, were observed both in one patient# J$ U2 p/ b2 P1 h( k
who relapsed and in one patient in remission. Our results suggest that the
) x C9 r0 Q! [8 r2 o: \5 \characteristics of complete molecular response on dasatinib treatment may be+ g; X2 M# Y& [& W8 j% A$ U* b: K& _
similar to that achieved with imatinib, at least in patients with adverse
( P* \: p% w/ U' L7 K' \8 X! S1 |disease features.' t' j# q+ J4 d! m+ P
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