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 a1 z# ^8 \( ]4 h$ l3 p: q- B
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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7 C8 R P: [- [* @( t. W作者:来自澳大利亚
5 v9 C) W) J- l' i+ F3 V9 Y来源:Haematologica. 2011.8.9.
5 Y$ y, k% {7 W3 sDear Group,
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; i- {- S" ?! V) [& HSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, @7 P4 F# d6 h" ^& i5 G D% etherapies. Here is a report from Australia on 3 patients who went off Sprycel f R* U- o' F3 G, P% N
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients% B! i4 g1 H0 x: u+ v" B
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
8 x6 }4 `& I4 {% ]does 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 failed7 \8 R' @/ G' h7 Z: n; _
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
; x( n( L* O7 _% @3 kdifferent from the stopping Gleevec trial in France which only targets patients! E* Y& L9 t4 \% u
who 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
2 Q6 }' n/ m1 Xresponse off Sprycel is sustained.. ?& n# \* Q& X, E6 q. X' l
7 X6 `3 T: i8 ]" J& t' sBest Wishes,9 [8 Z! d h! x8 n6 R
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
; b v4 G4 p+ {$ E |$ z! YDurable complete molecular remission of chronic myeloid leukemia following5 D9 O7 I' W# k( `/ w
dasatinib cessation, despite adverse disease features.0 p- P& e( E8 V. v0 m
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.# I8 u1 G P% I
Source3 s) q5 W/ n0 e0 b8 B
Adelaide, Australia;
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Abstract
; f y6 q5 e( O% o! cPatients with chronic myeloid leukemia, treated with imatinib, who have a4 [' x9 G) G e5 \
durable complete molecular response might remain in CMR after stopping
+ a& v; N& r, E1 wtreatment. Previous reports of patients stopping treatment in complete molecular
v7 T" `0 b2 w0 Z# t' Y2 u* D2 Nresponse have included only patients with a good response to imatinib. We
8 Y# I- x4 h& j0 j, `describe three patients with stable complete molecular response on dasatinib
( k# K+ I# ]/ S1 @# B+ gtreatment following imatinib failure. Two of the three patients remain in- d, M! A/ M( t
complete molecular response more than 12 months after stopping dasatinib. In' B+ d# _1 K6 u4 v* l, T) q. e
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to ]1 R4 Z* z* H( x9 H$ B* w
show that the leukemic clone remains detectable, as we have previously shown in" A! v$ q; U5 Z E2 G, F" \- M h* t; j
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 R4 k# m0 Z1 ~: W. Z
the emergence of clonal T cell populations, were observed both in one patient
$ P; A& x" R- P2 y" [- j1 Twho relapsed and in one patient in remission. Our results suggest that the
; x3 y. Z1 @. Q7 `& z3 Y3 a0 E. Vcharacteristics of complete molecular response on dasatinib treatment may be
- J" N! A3 c; ?similar to that achieved with imatinib, at least in patients with adverse
9 W" J# M1 B' X/ kdisease features.
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