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。
: b3 b- b: V2 y4 o' a 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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1 z3 _2 y3 G/ a9 j% R. c5 R, V* G作者:来自澳大利亚
8 c1 U \1 T) J4 B$ H来源:Haematologica. 2011.8.9.9 l0 T: v B3 Z6 t, j
Dear Group,- H& q' W1 j8 q3 i( D
6 U5 D* _6 k% A, q! [Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML4 P6 l. }* S0 K- F/ m
therapies. Here is a report from Australia on 3 patients who went off Sprycel* V+ l. U1 { W# j" T& A
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
. Z1 u- e( X, g, O) ^2 \- ^remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel, U$ M6 g" g* ]- U9 ]$ N# _
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 failed
) V, A8 i: Z$ CGleevec and Sprycel was their second TKI so they had resistant disease. This is
, U+ K7 r* i \( `8 j/ X0 H% ]different from the stopping Gleevec trial in France which only targets patients8 x& y, S7 U& C G
who have done well on Gleevec.) h3 ^3 N5 E% a/ S' S
+ {( m0 w0 {: t- cHopefully, the doctors will report on a larger study and long-term to see if the( @* A2 N7 I" B1 c4 [# }0 k
response off Sprycel is sustained.* O$ `+ U' B% @4 |6 e) B' u
9 Z! b$ i* Y9 R; ?Best Wishes,
( B* v5 ]! r. W* s, zAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]. _' J) b# k b
Durable complete molecular remission of chronic myeloid leukemia following5 n! ~0 k+ Y' i1 X/ y7 l0 W Z( c
dasatinib cessation, despite adverse disease features., C9 U' r& Q$ Q6 I
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
3 z/ L6 n1 |' ^) gSource
/ u, n8 X( u7 n* wAdelaide, Australia;
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: e9 S0 h1 l/ s/ ~2 R( ~- _Abstract
, T% y: r3 \* L, FPatients with chronic myeloid leukemia, treated with imatinib, who have a
! q C. v" v* v2 e4 idurable complete molecular response might remain in CMR after stopping
E6 r8 B9 f2 T( `& G6 \treatment. Previous reports of patients stopping treatment in complete molecular
0 x* w" D9 l; a, A- p& m# Hresponse have included only patients with a good response to imatinib. We
5 ?9 I; z# y4 K* j" l$ I% \) Ldescribe three patients with stable complete molecular response on dasatinib; J x. E' G2 C) f% C( a; \
treatment following imatinib failure. Two of the three patients remain in( g6 Z4 z* D6 R2 N
complete molecular response more than 12 months after stopping dasatinib. In
2 Z2 T1 s0 d1 Y+ M9 Z( tthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 g! @% Z3 `! s/ ^" M( \* r) Z( q
show that the leukemic clone remains detectable, as we have previously shown in
4 F- W% J7 `! C& E2 { q6 himatinib-treated patients. Dasatinib-associated immunological phenomena, such as3 W+ [* y- y2 D
the emergence of clonal T cell populations, were observed both in one patient
! ^$ n0 b- M0 o" }& j% k& y7 j" u. }/ u( awho relapsed and in one patient in remission. Our results suggest that the4 M. z! H% d- A
characteristics of complete molecular response on dasatinib treatment may be
$ L( B1 C6 n+ Z8 \, Esimilar to that achieved with imatinib, at least in patients with adverse/ ]0 D% t# n- h, c5 F# y1 I
disease features.
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