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。
1 ~: C. k; f! ^) ` 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$ m2 X8 W" @9 _
来源:Haematologica. 2011.8.9.
; l% ?; s5 W# D$ O5 o. a& C( i$ c, dDear Group,% m( \! Z, r) E" j V5 z, h
+ k4 R+ x4 U$ M( e$ G9 E' f, ZSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
* |. r% h! Z; qtherapies. Here is a report from Australia on 3 patients who went off Sprycel7 @& @ ?2 z+ p6 t% n0 e5 Q" b
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 ?+ {) ~- V+ h! Jremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
" I/ ^& c) h, n6 B# j( zdoes spike up the immune system so I hope more reports come out on this issue.
9 C1 j# X# ]5 @. `
2 P. X+ m# V, |The remarkable news about Sprycel cessation is that all 3 patients had failed% \+ U1 U8 I3 K7 I
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
+ L5 L8 ]9 g+ odifferent from the stopping Gleevec trial in France which only targets patients
/ L+ P, G! T( Q7 w% z' b ?who have done well on Gleevec.
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2 ~+ u s, h! V3 AHopefully, the doctors will report on a larger study and long-term to see if the2 H) t2 Q! R& S3 x; T; x
response off Sprycel is sustained.
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Best Wishes,
7 ~4 i2 c" J/ H. vAnjana
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4 t9 p- N8 L5 f8 dHaematologica. 2011 Aug 9. [Epub ahead of print]
( a$ J; ]" q" O8 C4 W1 f, tDurable complete molecular remission of chronic myeloid leukemia following
! }4 X# N5 d; ^0 Xdasatinib cessation, despite adverse disease features./ v* Z! C! O0 r
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;
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$ j. s; m a- l9 r% ]Abstract
8 K$ G2 W! u$ G0 s2 GPatients with chronic myeloid leukemia, treated with imatinib, who have a" `* S- f/ T+ q+ o5 {
durable complete molecular response might remain in CMR after stopping
4 \! [+ B' G- m' o; k! [treatment. Previous reports of patients stopping treatment in complete molecular2 W) T; @5 y* C X4 F# Q1 {
response have included only patients with a good response to imatinib. We, c5 J% ]5 n/ K
describe three patients with stable complete molecular response on dasatinib
5 f3 E, ^, H$ dtreatment following imatinib failure. Two of the three patients remain in
% M; J* b H) Ccomplete molecular response more than 12 months after stopping dasatinib. In
6 n5 C& J) c- q5 J5 l6 t2 Y) ythese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 m* Z4 w& |9 B! A3 Y1 }* u; h5 j
show that the leukemic clone remains detectable, as we have previously shown in
" S* m2 [- ^8 ~4 `1 o/ `& y# Fimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
- B/ H# ?/ ~$ X! y# b$ ythe emergence of clonal T cell populations, were observed both in one patient7 H3 ?$ x( |+ b$ U
who relapsed and in one patient in remission. Our results suggest that the
7 K, N* h; r6 D) _, ?, {- u7 |* Ucharacteristics of complete molecular response on dasatinib treatment may be
- H- f+ Z9 Y' h" ~1 s, @* R; ]similar to that achieved with imatinib, at least in patients with adverse
' p) p- k1 }4 Tdisease features.
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