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。' L- N1 K5 _' J0 E$ r9 ?- {
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。) t2 T6 U9 u, C1 T* i. E
" R+ f9 R/ [$ i( n) s+ S# `+ P! N0 d( }作者：来自澳大利亚
. F6 N) Z9 M! ^5 J来源：Haematologica. 2011.8.9.
% N' v! z7 { S7 I) e0 V$ fDear Group,
' Z# D& `* c( T; A: _
! m5 {/ W# a9 ^8 A% ?Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
" P! B8 s8 p7 P1 L+ B7 i! _: d+ ftherapies. Here is a report from Australia on 3 patients who went off Sprycel
, g# ], ~4 _3 f ~& Uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
# i0 @7 ]- @" H$ Wremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
. \2 b. g0 \) O) o& Zdoes spike up the immune system so I hope more reports come out on this issue.
$ }3 Y) a' z S( n) F" d# c$ t
+ N4 L2 [' K5 _3 {- q% B' iThe remarkable news about Sprycel cessation is that all 3 patients had failed
( V) E# S. D) y2 r. R, @% TGleevec and Sprycel was their second TKI so they had resistant disease. This is
6 g( V& q1 N+ t" Z: jdifferent from the stopping Gleevec trial in France which only targets patients/ p, a( I& `# O$ F& d+ P
who have done well on Gleevec.1 f6 a6 W9 }) ~+ `
! R! M8 H- f# X; RHopefully, the doctors will report on a larger study and long-term to see if the. M' e% U# {# [ N* r
response off Sprycel is sustained.
* g N$ _% Z4 D. \3 ^0 K3 [2 u( o, I+ I% ^4 J4 \+ G6 b
Best Wishes,) \4 D8 E4 P' b' d+ P
Anjana
6 N0 h4 @7 b$ ]6 N. w
/ R5 T8 i" p1 B0 l6 N q9 Y4 [: Y; u5 G
' C; u; f( ^9 u: a( hHaematologica. 2011 Aug 9. [Epub ahead of print]- \" r: E1 ? s7 B
Durable complete molecular remission of chronic myeloid leukemia following
6 q. [1 i2 I3 b1 j; l/ S) F8 C9 Idasatinib cessation, despite adverse disease features./ `+ ]) T5 y) \" v5 q
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.5 ~! B* c5 S+ y0 [' u5 [
Source: m% i, f! M/ a; M, x: M
Adelaide, Australia;% d' O% n* f. b# H
9 ^9 L+ V5 S" W6 E z
Abstract0 M g- p$ [0 G. `+ U. G" J% A
Patients with chronic myeloid leukemia, treated with imatinib, who have a
$ C# |: z# R* O0 d5 Z8 Odurable complete molecular response might remain in CMR after stopping5 ^$ d1 ~- N c- v- ]# q, [* O4 _2 @
treatment. Previous reports of patients stopping treatment in complete molecular3 Q. T3 c$ B, V$ c1 q- D
response have included only patients with a good response to imatinib. We+ h: ~6 w% N0 p) s+ n- t# ~
describe three patients with stable complete molecular response on dasatinib
0 X8 a2 [/ v. e6 W7 ]: ^treatment following imatinib failure. Two of the three patients remain in6 S( p* D- S# B T
complete molecular response more than 12 months after stopping dasatinib. In
6 I3 e v3 L* U, \* Jthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to7 Z! I2 n/ L+ J- ~" |! U1 e i* }
show that the leukemic clone remains detectable, as we have previously shown in
2 [) @) W; u, i5 \& Z( K3 a) b, Y1 a- Yimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
1 j8 k# ^ ?+ o2 ]& C4 `the emergence of clonal T cell populations, were observed both in one patient) ]* Y% B' G5 V; v$ {3 `% r
who relapsed and in one patient in remission. Our results suggest that the- m6 z1 m7 d, b! |2 k3 g
characteristics of complete molecular response on dasatinib treatment may be; \9 K1 {" b. L2 H4 z" i
similar to that achieved with imatinib, at least in patients with adverse5 {$ l5 ~* n2 h( R( e4 ^# e
disease features.
$ ?% A+ j7 i, C |
显身卡
