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。
+ {0 B# E; h7 z$ D/ i# E; m7 w* V0 h 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。
4 _5 y1 x" }) u1 ]: P, S6 w# s ) P4 V1 O% A t7 A
作者:来自澳大利亚9 U9 z/ p/ E1 K0 |
来源:Haematologica. 2011.8.9.
8 I7 s% I& C! A3 ?Dear Group,
8 c, c0 B7 L. g2 q0 o; r5 d5 `) f2 Q) X# j) x
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
5 g& @. Y* M) Z! [! k5 m( ]+ \/ ytherapies. Here is a report from Australia on 3 patients who went off Sprycel
9 P) Q- e4 y" |( I" Hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients+ f, K" @' V" N u! C6 H. p
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 O7 G! y. y; a& `
does spike up the immune system so I hope more reports come out on this issue.2 o6 X& O) _! l+ D5 H
+ S2 X% h% g5 g c2 X* ]! a
The remarkable news about Sprycel cessation is that all 3 patients had failed- [ `6 L3 u/ r$ ~ L/ h9 y4 U
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 U! l. s+ ?; U' S( D, n2 N* ^
different from the stopping Gleevec trial in France which only targets patients5 Q8 u) L& i4 f( @( f
who have done well on Gleevec.6 L. S" @. j- _; M
/ Q$ P m: G- s
Hopefully, the doctors will report on a larger study and long-term to see if the
- q9 r' R5 \% v. D/ K% B, |response off Sprycel is sustained.
( H" W+ @6 @# v1 ^1 x& d2 @+ p
: P% ~6 B" ~8 \7 YBest Wishes,3 E' o0 u% c8 u# c! |
Anjana
* G' F; h9 L7 e& J/ `. M
, d! w5 p- G! z, G( T& A/ ]
( B4 e9 I- \5 K2 a
: B( K% D( q8 X6 M5 |6 FHaematologica. 2011 Aug 9. [Epub ahead of print]& F/ r9 @2 D2 u' K: a4 I* U4 Y
Durable complete molecular remission of chronic myeloid leukemia following( N1 p/ w4 M2 y2 J" }( H
dasatinib cessation, despite adverse disease features.( u- ~3 E4 }) l* H: K$ n) ^
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
) A' J2 ^6 ~/ Q2 W" N0 y* xSource
4 _7 K: C0 I0 MAdelaide, Australia;9 R+ r7 r% a4 u" ]0 h0 y6 a0 z' f
, |, Q& a3 r% z+ u, g3 L" tAbstract/ f1 x7 O6 M; f( m
Patients with chronic myeloid leukemia, treated with imatinib, who have a* n0 _2 f5 P0 F* ]. }# W
durable complete molecular response might remain in CMR after stopping7 Q4 W9 U: P# `+ B' h
treatment. Previous reports of patients stopping treatment in complete molecular8 R9 L W( R3 ~2 b- z$ U
response have included only patients with a good response to imatinib. We. C& `( `4 z' {
describe three patients with stable complete molecular response on dasatinib
, N( q/ g: r& a2 ~ r+ D; utreatment following imatinib failure. Two of the three patients remain in& Y1 l- u2 I1 \& r
complete molecular response more than 12 months after stopping dasatinib. In
8 q2 G) E& e- e% Nthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
2 o0 S3 R! `$ x n- y nshow that the leukemic clone remains detectable, as we have previously shown in
& s$ p9 M* q) j. bimatinib-treated patients. Dasatinib-associated immunological phenomena, such as% D0 [# e2 v7 ]
the emergence of clonal T cell populations, were observed both in one patient
1 F/ y% Z3 h' mwho relapsed and in one patient in remission. Our results suggest that the
5 p% O) B6 J3 C( r3 ^* b* i2 q& mcharacteristics of complete molecular response on dasatinib treatment may be1 ^3 U( e# A0 b, C; W
similar to that achieved with imatinib, at least in patients with adverse
( w+ a# d- S5 T" w; `; j6 S( bdisease features.
' ?# w k" Y8 ?5 L( v0 F* ?4 W+ h |