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 J9 i) q- b7 V; W* t 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 X- \, t W! Y4 u # C( s: u# [5 m$ x+ x3 @4 r1 u
作者：来自澳大利亚
3 J! s# A- w: I% {. ^来源：Haematologica. 2011.8.9.8 p& b% O, y5 N
Dear Group,
& l f3 d; s+ \$ y" M* h- {. n/ [, r0 M. p9 s: x7 S& h8 e
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" J+ z. U, R6 V; K0 O9 h
therapies. Here is a report from Australia on 3 patients who went off Sprycel
- }. [( D+ `: L+ ^) K, Z* dafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients( l# ` i7 |* A" j- w! v' q/ ^
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
. ?6 R5 l* E5 o; C0 G/ tdoes spike up the immune system so I hope more reports come out on this issue.
[5 y$ P4 J; ~5 W( q+ S0 E- i* m2 A0 e5 B% z8 U- s7 C1 d
The remarkable news about Sprycel cessation is that all 3 patients had failed
; _. y2 P, b( FGleevec and Sprycel was their second TKI so they had resistant disease. This is
# N) U% B9 K& n$ l. Vdifferent from the stopping Gleevec trial in France which only targets patients' _: N+ [% e: W+ o. b: w5 @1 x: J! A
who have done well on Gleevec.
7 F6 O2 y4 L2 W
; ?8 u7 z- h! k2 S* YHopefully, the doctors will report on a larger study and long-term to see if the
% a: x9 ]4 j. Q1 b+ oresponse off Sprycel is sustained.
2 Q7 W8 w/ B1 K* k. v4 A
: F+ a& A6 Z4 F# o' E" O/ E; dBest Wishes,
5 V3 e- @4 F. U5 BAnjana
4 N. o) ]& l1 k2 Y0 {
& X7 C6 w6 O% R. v. n9 M4 z3 ?( o- F
: T( D! A+ z% A; E# d3 r. O* q( p1 l3 V+ N7 |* k
Haematologica. 2011 Aug 9. [Epub ahead of print]
" o, u7 w. R3 y3 m2 G2 _- p, pDurable complete molecular remission of chronic myeloid leukemia following5 [) s+ g- N) L& e' o9 E! o4 `
dasatinib cessation, despite adverse disease features.2 d& V6 Y- F0 o" w9 |4 I
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
0 H6 a6 c& b) [3 g; KSource B8 I! I$ ?' O) ^8 L l' _
Adelaide, Australia;/ ]+ Q# `1 M! X2 u+ f. y2 h9 R
4 W$ E c/ f( _5 j9 gAbstract
- C+ J# Q) K+ K/ T! o8 w, VPatients with chronic myeloid leukemia, treated with imatinib, who have a* k! A) u; R" p6 p8 u2 p% Q
durable complete molecular response might remain in CMR after stopping8 j6 v1 K7 }, |6 o+ ?+ Y
treatment. Previous reports of patients stopping treatment in complete molecular
1 p5 A/ i) H( ?1 V/ j7 x) H1 g9 Zresponse have included only patients with a good response to imatinib. We2 p* ^8 A' N0 K; `
describe three patients with stable complete molecular response on dasatinib
) m( y1 s9 D! \3 W3 V% h1 Gtreatment following imatinib failure. Two of the three patients remain in
$ t6 y7 u" l% p9 bcomplete molecular response more than 12 months after stopping dasatinib. In& B3 I; q( v5 A! D ~/ ~' }
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
7 j; P8 k+ }, N" [. Z+ @+ Cshow that the leukemic clone remains detectable, as we have previously shown in3 a/ W: [* {! D
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ X# U+ ]6 H6 T% }) Gthe emergence of clonal T cell populations, were observed both in one patient2 s) ?. o) {0 Y5 f
who relapsed and in one patient in remission. Our results suggest that the
( o( C" f1 U/ @% p1 c0 W& Z N8 a" icharacteristics of complete molecular response on dasatinib treatment may be
$ x' g! h" ]1 a! asimilar to that achieved with imatinib, at least in patients with adverse
& ^, j @* U' C' mdisease features.) r- ~4 D: B+ j3 m
|
显身卡
