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。" i1 S' E7 S! f H/ l
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' H5 K+ N+ Y7 T5 r+ ?' D
来源:Haematologica. 2011.8.9.
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9 D2 l P' ?# M& iSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML! D S, _3 { Z# ` q4 K7 ?
therapies. Here is a report from Australia on 3 patients who went off Sprycel
6 |% v9 K) t+ Cafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
W: r7 N# w/ premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
: F2 N) p5 G! P0 m; q6 B- G4 ~does spike up the immune system so I hope more reports come out on this issue.( e) ^/ s- M; {1 C
M1 d- L2 [( q7 A' OThe remarkable news about Sprycel cessation is that all 3 patients had failed
; R4 g3 D4 o6 @( V2 eGleevec and Sprycel was their second TKI so they had resistant disease. This is
# g' z A3 E" Q" L: u% zdifferent from the stopping Gleevec trial in France which only targets patients/ \- B2 x+ P- W/ }4 i5 X
who have done well on Gleevec.6 q2 Y! C7 W* Z6 R2 ?5 J7 b( l( w( `
V; W' r$ N. q- _5 k8 GHopefully, the doctors will report on a larger study and long-term to see if the# K( N! w6 H' O4 n2 f \; s
response off Sprycel is sustained.* @6 M4 Q3 f. ^" {& Z/ C% k+ h
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Best Wishes,! {1 R: F o. _0 _7 E R
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
q, c# k9 _0 I# a" xDurable complete molecular remission of chronic myeloid leukemia following; s3 ?* a/ p4 X! I8 K d$ j
dasatinib cessation, despite adverse disease features.
/ g! Y2 W8 j9 P& u4 mRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
/ F2 t* ~( s; |( g* YSource# I, {- M/ j/ T7 t' k9 U$ B: i
Adelaide, Australia;/ r( K4 Y7 h, t f) j8 N& u; |- ]
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Abstract, {# E7 u# F0 r( a/ O& J7 N
Patients with chronic myeloid leukemia, treated with imatinib, who have a
; {$ [5 n E3 Pdurable complete molecular response might remain in CMR after stopping6 B; _, u7 C/ B) `5 J% r
treatment. Previous reports of patients stopping treatment in complete molecular
4 v# c5 q/ y, w& V( L5 nresponse have included only patients with a good response to imatinib. We' |5 m5 Q; F8 K
describe three patients with stable complete molecular response on dasatinib4 t0 m/ R. \. X( K
treatment following imatinib failure. Two of the three patients remain in
+ T X% c- w( u2 z9 V# K( Ocomplete molecular response more than 12 months after stopping dasatinib. In* w0 T+ v7 c& ]* O
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to9 t$ T7 |" y: L( R) S
show that the leukemic clone remains detectable, as we have previously shown in$ ]5 ?3 k1 w! X# @; s- b
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- n' E6 Z- R9 B7 T
the emergence of clonal T cell populations, were observed both in one patient
3 o! x1 @" x$ X2 [; Lwho relapsed and in one patient in remission. Our results suggest that the
& g) f' T+ b' k- N) d8 kcharacteristics of complete molecular response on dasatinib treatment may be
- G/ ]6 W: ?8 d! g7 ~similar to that achieved with imatinib, at least in patients with adverse
h# `' J+ y5 @: T. y" [7 B6 ddisease features.+ `6 r$ O0 m* W; }! G+ N
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