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。
8 P9 A6 W. R6 ` 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。! a- K% X+ G6 `8 N
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作者:来自澳大利亚7 J; F# x+ b6 N u) r9 o7 R* m7 b
来源:Haematologica. 2011.8.9., M8 I. T+ y: }- v
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML; K' \: v( c T8 _# I: S
therapies. Here is a report from Australia on 3 patients who went off Sprycel) h8 E' a5 E8 T0 g# t) Y4 `% O
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients5 m: u5 \3 ^4 I3 ]+ c
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
. {( \) ?4 u& J$ jdoes spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed
3 n7 y3 P( k, i# O. N2 TGleevec and Sprycel was their second TKI so they had resistant disease. This is
6 m* ]$ g' h, ^( i4 A) Udifferent from the stopping Gleevec trial in France which only targets patients
' K8 j8 J' D0 z1 I" n3 U* G+ C7 Cwho have done well on Gleevec.
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; v0 N" [9 E2 ^8 H# RHopefully, the doctors will report on a larger study and long-term to see if the7 x" {* b3 ]( e0 b9 {
response off Sprycel is sustained.
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1 D6 I) S5 _( V% \: UBest Wishes,
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Haematologica. 2011 Aug 9. [Epub ahead of print]0 v3 m" d$ g/ K, ?
Durable complete molecular remission of chronic myeloid leukemia following
$ \1 c4 c" f u5 q( x9 P0 mdasatinib cessation, despite adverse disease features.1 B$ w/ }( r! U$ {3 c2 b3 w; v4 ]
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
1 a q+ t {9 w/ G% p0 W& CSource
; t; E9 d; m- ]3 e2 HAdelaide, Australia;( I& t: m# e- m. Y& ^. D
& t5 P! i# X4 o" \$ tAbstract4 @4 [" i) [: M0 C$ I
Patients with chronic myeloid leukemia, treated with imatinib, who have a
* Q+ O* S! L' y/ Q0 U0 Z: l. Edurable complete molecular response might remain in CMR after stopping
3 t9 i: {& l1 b1 [* X9 _+ l, Vtreatment. Previous reports of patients stopping treatment in complete molecular
/ N$ Z2 ~# s6 h ^7 [1 z% ~4 \( Xresponse have included only patients with a good response to imatinib. We( t4 }% B3 T7 I2 B
describe three patients with stable complete molecular response on dasatinib
% s6 i1 H8 L1 u1 Z" atreatment following imatinib failure. Two of the three patients remain in
" c- h& j/ W# a: P( i% g8 f5 ?8 Lcomplete molecular response more than 12 months after stopping dasatinib. In1 O/ {$ q2 F9 h/ T5 g, q
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
& m( W7 k+ Z, w2 h/ l, F Gshow that the leukemic clone remains detectable, as we have previously shown in
5 b3 a* {6 K, k7 ?$ j- ]* simatinib-treated patients. Dasatinib-associated immunological phenomena, such as7 W% e' D# v$ Q1 {7 P& A
the emergence of clonal T cell populations, were observed both in one patient
; \) J. m. ]; f! ]+ Jwho relapsed and in one patient in remission. Our results suggest that the
R; j6 ~4 S i1 i5 @6 Echaracteristics of complete molecular response on dasatinib treatment may be
7 u+ M! x: B" j6 B9 U) Ksimilar to that achieved with imatinib, at least in patients with adverse, e, r/ w' l" k9 m) I
disease features.1 D$ f+ e+ f8 A1 {3 I9 ]: Y
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