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。
. e: {' a, j8 K6 m 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。& X0 I$ m" E6 m8 Z
5 V* `! H2 l k5 `; f$ F作者:来自澳大利亚
' V" m6 k5 w* w* V0 k来源:Haematologica. 2011.8.9.& i& L' {0 y5 |# A$ }+ b
Dear Group,& a+ [6 I0 @: N$ Z+ z: Q
# M$ f8 p( r! |+ f' d& j( N8 oSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
* K/ O& E2 J# R) l! G. H8 ltherapies. Here is a report from Australia on 3 patients who went off Sprycel
2 z+ v( W' Y2 b1 xafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients7 @7 z6 |% c" W: e U! {
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel- T+ I; p H8 U1 c9 Z0 U
does spike up the immune system so I hope more reports come out on this issue.
3 k: I# Y; `( W6 P% ~* c% m
" N# [, k( T' v8 d9 W7 _" d7 WThe remarkable news about Sprycel cessation is that all 3 patients had failed
! {# i& y# P8 }5 A kGleevec and Sprycel was their second TKI so they had resistant disease. This is( {4 g G# `" W9 | t4 T/ q6 e
different from the stopping Gleevec trial in France which only targets patients
}2 @ g, K. y4 Y4 Mwho have done well on Gleevec.
3 {" g1 H: }% f
3 n+ W7 q% h$ C* G( m' W0 dHopefully, the doctors will report on a larger study and long-term to see if the
# w& \; z; R D# |% N7 tresponse off Sprycel is sustained." p0 A% Y) k, R. W2 x
& [- }+ A/ O7 T9 k5 R1 u4 C
Best Wishes,
6 r0 g0 ]/ L O' _- `& j" HAnjana; ~3 i+ Y3 ]: g$ j5 C t6 z
& d6 R# c! r) T/ G C6 d/ e5 ^8 o+ A! v; }/ ]* L
1 N. y& G" N$ d$ E" z& ^Haematologica. 2011 Aug 9. [Epub ahead of print]3 U1 [1 M; J3 s5 E" |+ C
Durable complete molecular remission of chronic myeloid leukemia following5 W& {/ v( J1 e6 ^$ c: q) { l
dasatinib cessation, despite adverse disease features.9 m' l9 B8 F/ V3 k* v3 g" c
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.. T8 o0 K {3 Z+ f& h; a
Source
* q# c# V) Q- F, MAdelaide, Australia;
; j6 C, z2 a9 O- d& o! j$ s" y) P) \: p/ g+ k z9 O: H! d
Abstract$ O, z6 H' T# v& t# e
Patients with chronic myeloid leukemia, treated with imatinib, who have a( k3 q, {( c" ^
durable complete molecular response might remain in CMR after stopping, D# Q' H' ^) n! s6 i9 G
treatment. Previous reports of patients stopping treatment in complete molecular
6 i2 o; c: Y+ l* Mresponse have included only patients with a good response to imatinib. We
6 ]! K) O+ P) R: Y4 m3 w1 x+ Adescribe three patients with stable complete molecular response on dasatinib
6 B: S1 H8 ^% o9 n; M2 }5 Ptreatment following imatinib failure. Two of the three patients remain in# ?1 g+ o) ~7 I8 O
complete molecular response more than 12 months after stopping dasatinib. In
$ i0 {5 P' D) Z# |these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) }0 @+ \* S& g% ~) @% xshow that the leukemic clone remains detectable, as we have previously shown in0 }3 h; X c# H; m, u" B& d. s: T
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as; ~% i3 t6 z! _/ }6 H! g
the emergence of clonal T cell populations, were observed both in one patient' S: M/ p" z! H, W. B; O( B
who relapsed and in one patient in remission. Our results suggest that the
1 S, D7 C$ I2 V1 Kcharacteristics of complete molecular response on dasatinib treatment may be; J+ e8 O4 K s
similar to that achieved with imatinib, at least in patients with adverse
9 o, W) ]8 _6 F$ {" C: kdisease features.
, [" } O( L' K6 K! H" {+ \ |