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。
- w: s2 n& D+ {1 K 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。) W3 `" S+ K* s6 S
f/ o" [1 V6 x. n
作者：来自澳大利亚
5 }9 [. K7 a4 B, [来源：Haematologica. 2011.8.9.
. c/ d7 E3 y) ~$ Y% ]2 P0 m+ g$ eDear Group,2 ?: @! b1 h9 Q
: x" X M( m, ~- D& R, t8 rSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML$ J# a+ y* ]" |& K) h
therapies. Here is a report from Australia on 3 patients who went off Sprycel
4 n' } g1 D% N9 [after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
/ i2 z) A+ Q( v0 [- s/ r. Jremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
! q3 E3 f6 j$ t! F% {does spike up the immune system so I hope more reports come out on this issue.( b9 \9 X6 i! y" F
( w5 T/ ~, ]# g% ~5 J$ l+ cThe remarkable news about Sprycel cessation is that all 3 patients had failed& e$ E3 A% j1 r! k, K- s% b% c2 G3 W
Gleevec and Sprycel was their second TKI so they had resistant disease. This is5 p7 I$ _( V5 K! f
different from the stopping Gleevec trial in France which only targets patients
1 [8 C. o& g5 Q) L! y6 }who have done well on Gleevec.
3 O, T. [ Q& T$ b: j& W
+ h' x3 \4 I. h( I' DHopefully, the doctors will report on a larger study and long-term to see if the
: |# w3 x0 i7 S! D" Vresponse off Sprycel is sustained.
4 A, @2 R. E" W* K8 r2 S
8 n1 o2 S: Z% d2 {) ?/ NBest Wishes,/ ?+ H. V: Q- C/ j. |3 V2 S
Anjana
7 \% w& q, H6 Y( p1 p1 i$ p7 Z3 [4 E! w/ C. }- o
4 h1 H! S1 Z. v& ?, v o
$ Q$ ]5 H; U6 y$ kHaematologica. 2011 Aug 9. [Epub ahead of print]
+ h3 n) M4 x5 F" o/ I, ^3 `Durable complete molecular remission of chronic myeloid leukemia following1 c% ?, ?* a7 A
dasatinib cessation, despite adverse disease features.1 O. ?* r" r7 X$ b( R. C* N. ?
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
6 _% ]: e1 u. `6 LSource7 Z3 _/ h9 ?- Q* h
Adelaide, Australia;7 S! c* A5 N5 Z7 s2 o4 p7 m- J
% V0 c) E& c% b5 V* @2 ]! J. ^
Abstract9 b/ h* A# U+ C) k) K( ^
Patients with chronic myeloid leukemia, treated with imatinib, who have a
/ _5 j5 s; N; P9 O1 [durable complete molecular response might remain in CMR after stopping
( g8 C4 T" |2 w5 R# ltreatment. Previous reports of patients stopping treatment in complete molecular
: @# f F! v1 H7 e& Gresponse have included only patients with a good response to imatinib. We
0 k2 `& A$ E1 A/ K" F! }, `: N1 G. Ldescribe three patients with stable complete molecular response on dasatinib
0 c4 M+ q+ p+ M Q. J; c$ L' }treatment following imatinib failure. Two of the three patients remain in+ Y9 m' d, T# b1 W. W
complete molecular response more than 12 months after stopping dasatinib. In5 \3 b8 P) T/ E) Q
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
: I$ U) R- \3 B. [show that the leukemic clone remains detectable, as we have previously shown in o' r, d; t- s2 d: J2 u
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as6 ?' w9 r" w0 X7 C7 K0 M
the emergence of clonal T cell populations, were observed both in one patient
$ |( k2 j3 Z. a+ D$ @who relapsed and in one patient in remission. Our results suggest that the
( p: a2 D5 z, Z5 V+ gcharacteristics of complete molecular response on dasatinib treatment may be7 c- C+ A! D1 Z9 A& K
similar to that achieved with imatinib, at least in patients with adverse5 S; W9 V* y6 \6 n
disease features.
/ p; }7 H/ q. h P5 m |
显身卡
