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。$ O1 O$ D/ s" O7 v5 s& R' c
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。
+ p; e# y8 g+ ~" v# Z5 \& [" @% K* y
, D; x! F: D& ]3 z% c: T( h& z作者:来自澳大利亚
; N# o) F2 w; |来源:Haematologica. 2011.8.9.
" [# h9 r, f9 ?3 TDear Group,
& V4 Y0 S. E: E
4 S# } I# {; F3 m2 u5 M- V1 G2 BSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
) |, s3 R' \, I2 ] G- L0 Ktherapies. Here is a report from Australia on 3 patients who went off Sprycel
* }: z$ ^+ e' G, D' v( ? H8 `after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients' J* R0 @% G1 G6 V
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel ]7 f6 R [/ i) E
does spike up the immune system so I hope more reports come out on this issue.
# @" D1 X1 t9 n* Y( ]/ L& U( N2 Y
The remarkable news about Sprycel cessation is that all 3 patients had failed# R3 h: X: y+ h/ G9 s( Q. Y5 K
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
* j. u: C) j9 i/ C. n1 Y- Bdifferent from the stopping Gleevec trial in France which only targets patients
6 W( Z( q" G1 l3 e" i7 o# a6 hwho have done well on Gleevec.
+ Y8 }! b8 i8 Y0 K: F
$ X" I' Z+ \: N: W$ R/ `Hopefully, the doctors will report on a larger study and long-term to see if the
7 b5 k. `. W3 k% _response off Sprycel is sustained.
4 V/ t5 n( c5 Q; I4 ~3 n
% ?6 h9 b) Z# S1 q0 i% z gBest Wishes, T1 @) r, |" y( b
Anjana6 Q4 N3 f4 P' m) o
$ b8 v6 R$ e& Z- K' k1 D2 V6 Y: _+ D. _
0 |+ e. M3 }: _4 w" s/ I: CHaematologica. 2011 Aug 9. [Epub ahead of print]
! }4 z$ Q1 ]9 t9 g2 S* b% |Durable complete molecular remission of chronic myeloid leukemia following
% H4 @6 a# W9 P; v+ p0 [5 \dasatinib cessation, despite adverse disease features.* W% h0 l0 s2 b7 S$ |! d6 H
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' _: s6 T5 x. |% U
Source3 U3 s( U) a9 \+ H
Adelaide, Australia;
0 K2 S7 z- c& G/ c& Z n( P$ p, f. c9 \7 r+ c1 v) t
Abstract
6 A. {1 u( S$ [' M3 r$ iPatients with chronic myeloid leukemia, treated with imatinib, who have a; e6 r" R# y# ?) f/ z# J
durable complete molecular response might remain in CMR after stopping
6 y/ L: d9 l, o; Gtreatment. Previous reports of patients stopping treatment in complete molecular2 y4 x4 G0 t+ q
response have included only patients with a good response to imatinib. We
& v* U5 `/ M& @ K# _describe three patients with stable complete molecular response on dasatinib1 j r; d5 z- W1 a* Y5 |
treatment following imatinib failure. Two of the three patients remain in. P. ~& C: N2 c
complete molecular response more than 12 months after stopping dasatinib. In# Z+ w0 h9 u% c/ }# ^) h9 x
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to% f1 ~2 }& x4 m3 s8 o
show that the leukemic clone remains detectable, as we have previously shown in
6 l! d2 \$ i, Z {imatinib-treated patients. Dasatinib-associated immunological phenomena, such as1 R: d0 c) n. w- s$ v+ Y; C
the emergence of clonal T cell populations, were observed both in one patient, M: L- F* W" G5 w
who relapsed and in one patient in remission. Our results suggest that the/ B8 k6 S0 I! U w& |( o
characteristics of complete molecular response on dasatinib treatment may be
6 @) r1 ^, A& p/ tsimilar to that achieved with imatinib, at least in patients with adverse/ ]: E; v! c2 v( C; S3 F: y
disease features.; h6 @& ^8 S( Y. ?/ m8 b* H o
|