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。
* H( p5 D4 @2 `, e( L5 I 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。! B; r0 b8 \# N4 B( D5 w
% |, f( [) J) h! P7 d# w作者：来自澳大利亚
; ]: P) w+ i" D8 X% b5 t! A来源：Haematologica. 2011.8.9.1 W- ~8 C- ]2 O& `1 H" W2 l( g
Dear Group,
( a! c' A Q1 Z3 E. \( U' `0 \
|/ o4 L* E- e. p9 ^0 N) ZSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML6 _8 S: P5 B8 s1 H6 s4 O4 t
therapies. Here is a report from Australia on 3 patients who went off Sprycel9 K" B5 n; M# f4 X1 ]- r
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
8 ^- j4 S: D; l. W* Premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel7 P/ ^1 V+ E4 F1 ]+ h
does spike up the immune system so I hope more reports come out on this issue.1 n+ X \' ~- v; q
3 n6 h6 [2 g& N. h/ a
The remarkable news about Sprycel cessation is that all 3 patients had failed6 h: D! O$ b# s% U" X
Gleevec and Sprycel was their second TKI so they had resistant disease. This is6 d, Y' y' z- _! k5 ]* Y5 `3 A* @8 O
different from the stopping Gleevec trial in France which only targets patients2 N9 ^" w- W, j5 R7 C, Q( X5 e6 w
who have done well on Gleevec.$ G4 y$ g, P$ b" C7 j; w* a0 \
" U1 @& s1 ^! ]; C/ x7 ~/ ^
Hopefully, the doctors will report on a larger study and long-term to see if the
9 o+ w0 c7 s3 L7 x" vresponse off Sprycel is sustained.9 Z8 u) N' L- Q" p0 G, W
# W7 m7 G0 {8 u' }! {, S( B
Best Wishes,* m8 r( K1 ^6 \3 @( X1 f
Anjana: X- I- a4 l$ Y) v7 E# M0 }8 e9 r
3 ^7 O6 C' U5 k1 [2 s6 Z! U- v
* q s) h6 V. J/ M
% G7 i! J( ]) `Haematologica. 2011 Aug 9. [Epub ahead of print]! W! c2 k P" f. f3 V
Durable complete molecular remission of chronic myeloid leukemia following
- U0 K( U" d5 \+ {3 _+ ]dasatinib cessation, despite adverse disease features.& ? l) G# y2 O, Y
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.& ^4 v4 k+ a! |9 l
Source5 J6 D9 u$ `. j6 f2 ]0 ~7 u
Adelaide, Australia;
8 }0 ^1 z' a5 p* b# i' F% r( a) {* b/ o! Z, p
Abstract
6 z4 t. H9 o+ H( Y" z# z# lPatients with chronic myeloid leukemia, treated with imatinib, who have a
. R4 U4 p7 R. k+ l9 R+ n9 ^durable complete molecular response might remain in CMR after stopping$ U* k' l# D' Z
treatment. Previous reports of patients stopping treatment in complete molecular1 z+ L4 z E0 a; r
response have included only patients with a good response to imatinib. We
: F: \0 E9 z" gdescribe three patients with stable complete molecular response on dasatinib( V) t$ Y* C! m
treatment following imatinib failure. Two of the three patients remain in
$ I% R+ T; l0 mcomplete molecular response more than 12 months after stopping dasatinib. In
8 f5 R% G% Z- ]. L+ w! g' f; kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to% a$ ^0 l) X5 B/ {0 L) d
show that the leukemic clone remains detectable, as we have previously shown in+ z* \) N: A) r5 g
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
' {+ N; P7 C5 J6 V9 gthe emergence of clonal T cell populations, were observed both in one patient
" f% c6 L2 V9 Iwho relapsed and in one patient in remission. Our results suggest that the5 B9 F K7 X* o r% e
characteristics of complete molecular response on dasatinib treatment may be) T7 s6 }# }$ O9 F
similar to that achieved with imatinib, at least in patients with adverse
{, o$ K e/ E4 D- _- d1 hdisease features.
1 ^+ @6 V% j* x/ J; U |
显身卡
