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。
/ j5 S) h$ b0 d5 g. p, x5 L8 F 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。5 M6 u+ m) h/ q/ E. Z7 P7 K
6 A9 t# B0 r3 I5 w/ K: d
作者:来自澳大利亚
7 j" A/ ~; f& @2 Q$ c6 |; J" a来源:Haematologica. 2011.8.9.. u( e2 @$ Q: z& V5 v% U8 `
Dear Group,7 P1 G+ O8 n, Q+ t
) D9 ~ c. e# @: k- s/ s, ^* PSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
* |+ X6 }, T; g, s! K: ]4 K- wtherapies. Here is a report from Australia on 3 patients who went off Sprycel
: |7 _ Z; p: A* |after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, _/ C2 G% z3 ]remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
* G/ E0 K/ t) I( N! E: Adoes spike up the immune system so I hope more reports come out on this issue.7 j {. u6 ]% t1 f" i3 n
9 ~5 u) R6 R: D5 s* v$ k. r8 B* IThe remarkable news about Sprycel cessation is that all 3 patients had failed( Q6 C# w; G7 ]( U: \
Gleevec and Sprycel was their second TKI so they had resistant disease. This is' z( ?& o/ R$ X" y
different from the stopping Gleevec trial in France which only targets patients! O- W0 `& j& n [' n6 _
who have done well on Gleevec.) o* D! J1 g' n- r. b' w
- U: B7 ~: t; q6 y" z) k) O
Hopefully, the doctors will report on a larger study and long-term to see if the1 E& a: q* E4 ]. S. c0 W1 Z9 f3 z
response off Sprycel is sustained.
/ \3 J: C! F4 Q& C2 ~
" T2 D# `6 @0 A" J# j- LBest Wishes,$ O) Y$ G# u% c# Q4 t8 ~
Anjana; }+ ?4 X& j$ ^6 |2 z) R6 ~/ n. O
5 ]5 u0 u0 e9 F5 P! _8 g" i
' O7 u* b/ j0 V
( x% E; k: _& f) R$ ~Haematologica. 2011 Aug 9. [Epub ahead of print]5 ~. i3 m, k u# _) o6 s
Durable complete molecular remission of chronic myeloid leukemia following
% p9 c0 e( A% x$ rdasatinib cessation, despite adverse disease features.
, b# S" G8 q. E. r8 ^Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.; s0 y& n! T+ |* a& E! L( ]; F; b
Source5 w0 B+ U% T' h0 U: ?
Adelaide, Australia;
* Z( J. }; I$ H( w5 S) K0 S0 v: `2 q! m) A
Abstract
' h, j. k" d& V5 x, r9 zPatients with chronic myeloid leukemia, treated with imatinib, who have a2 @: Q& Y4 o0 [9 R- L
durable complete molecular response might remain in CMR after stopping
" i% Q( R" f. t$ Xtreatment. Previous reports of patients stopping treatment in complete molecular% v; w$ a I; G7 z1 s0 Z: _. q% f: V5 A
response have included only patients with a good response to imatinib. We# e/ \( ?. j9 A6 K& t
describe three patients with stable complete molecular response on dasatinib
H! g+ r& s% z8 p- Ttreatment following imatinib failure. Two of the three patients remain in/ v- n8 m8 _: {8 i$ s
complete molecular response more than 12 months after stopping dasatinib. In
+ z5 i4 A+ o3 S9 K$ ^% {these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
; t/ E- Q: a% O8 nshow that the leukemic clone remains detectable, as we have previously shown in
! [7 u- O0 ~6 V/ uimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
; u" {: v ^/ @' Z' } kthe emergence of clonal T cell populations, were observed both in one patient
W# ^; i( _) M1 [' Y Gwho relapsed and in one patient in remission. Our results suggest that the* p7 {9 o6 Z& X8 K( G
characteristics of complete molecular response on dasatinib treatment may be0 d; O( {' v. |7 t9 T
similar to that achieved with imatinib, at least in patients with adverse) [' _. E3 Z6 U+ X
disease features.
) c0 G. h. z f& G- ` |