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。
2 @& I# e" b7 t+ i9 Y 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。. H* f; m% M% L3 h( U8 J# D
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作者:来自澳大利亚
- ^1 J/ H5 x3 n$ b( Y2 P! n2 f来源:Haematologica. 2011.8.9.
+ e- f& b1 l( ?: eDear Group, t; @* L5 |7 i, n2 H5 ~7 f. s' w
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML; j; N# s8 z' s6 g/ F1 w
therapies. Here is a report from Australia on 3 patients who went off Sprycel
+ s& \2 E5 ], \4 G( Oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 v0 J% f+ B5 c( s! Gremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 ]8 c" }* E4 n7 P% ]: t$ mdoes spike up the immune system so I hope more reports come out on this issue.
8 } { M- A$ z& L. l7 ]9 H$ m3 c
- ~5 L: d( u5 s' L7 h! I9 tThe remarkable news about Sprycel cessation is that all 3 patients had failed
* G2 R6 t% V' `, `1 h" W3 P- RGleevec and Sprycel was their second TKI so they had resistant disease. This is/ w+ r1 m/ B3 Y+ Y; h' S/ @3 g
different from the stopping Gleevec trial in France which only targets patients
! r$ ]$ O2 C3 Z9 Vwho have done well on Gleevec.! q3 r4 i7 j" w
8 Y' k" r9 X+ h5 MHopefully, the doctors will report on a larger study and long-term to see if the
% @ W. l) g) M" B- N6 O5 m8 i/ cresponse off Sprycel is sustained.
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" g, |! P. R) l8 h- ABest Wishes,
+ C8 p$ [/ ~1 V, ^ tAnjana3 x( ^5 a' _* D% T8 B% p& U" z
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4 f8 e! P; r0 x, |+ h# HHaematologica. 2011 Aug 9. [Epub ahead of print]& B% y6 a+ l+ Y' D
Durable complete molecular remission of chronic myeloid leukemia following; n V5 b+ }5 [8 V/ m
dasatinib cessation, despite adverse disease features.0 d& E% P5 {6 p
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.4 Z) L" J2 c6 c: G
Source
6 z1 z9 g3 L7 T, OAdelaide, Australia; _7 w( g, H6 c3 S: i. s! Y
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Abstract
T7 p- r( z" Q) X& J& xPatients with chronic myeloid leukemia, treated with imatinib, who have a
/ O1 `( v& l( o0 t4 p! k* ]( U. M/ gdurable complete molecular response might remain in CMR after stopping
8 V4 T0 V0 r7 B3 w! Y# L1 _% g. ztreatment. Previous reports of patients stopping treatment in complete molecular
E3 x+ v; |1 b6 P: a: Zresponse have included only patients with a good response to imatinib. We
7 }% z, H- |( s3 qdescribe three patients with stable complete molecular response on dasatinib. o& \4 f9 j* N1 Z3 Z0 \4 f; o
treatment following imatinib failure. Two of the three patients remain in
) u9 ^% l# c# g$ J$ u$ c0 Kcomplete molecular response more than 12 months after stopping dasatinib. In: r: G U, p7 I' h& v$ L9 w$ _/ R5 P
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
( O, l0 P) A, h2 K h' @show that the leukemic clone remains detectable, as we have previously shown in9 Q9 X/ L/ u2 J) n% Y
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as) ]# N* P7 E$ s( G( |
the emergence of clonal T cell populations, were observed both in one patient8 m ~- t" n8 }. q6 a3 x
who relapsed and in one patient in remission. Our results suggest that the4 G/ f5 f% J, s R. r
characteristics of complete molecular response on dasatinib treatment may be! P2 O( d3 D7 {# T
similar to that achieved with imatinib, at least in patients with adverse) e6 |8 r. i8 ?# N* t& S
disease features.2 n1 y) E! v, U! Y4 v* H
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