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。
8 L& U. {% s! f: v* K6 z. O i( v 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& q0 u& ~+ }+ e
6 f/ g, I! m1 V2 A# K作者：来自澳大利亚" v' \& W {0 n# `- k7 S
来源：Haematologica. 2011.8.9.: d* v {' l b- ?! J/ g
Dear Group,! {. t/ n9 e3 J: `7 Q
: H O7 t4 K% U# D a7 L% W1 `Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" s1 N5 Q5 ~3 l% d" r+ p- X: Q _3 Y/ v
therapies. Here is a report from Australia on 3 patients who went off Sprycel
6 g1 b' p+ w6 i2 U6 c c. X0 A% mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, v4 p2 U3 [" ?8 X; g& Yremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' i3 R; F( g/ D0 R
does spike up the immune system so I hope more reports come out on this issue.6 k! e* s( R& g `2 L9 j; Y0 h5 f: s
* {2 |4 B- ^+ C: K2 P' a( aThe remarkable news about Sprycel cessation is that all 3 patients had failed
- A( z n9 e9 b( x8 CGleevec and Sprycel was their second TKI so they had resistant disease. This is
$ K9 N. X$ _7 w4 Sdifferent from the stopping Gleevec trial in France which only targets patients
2 c( _* A$ n1 Q6 |/ Kwho have done well on Gleevec.
' g/ B" h( \$ } X, t$ j
, a( m, O9 E7 R% [0 Z, B6 y$ ^Hopefully, the doctors will report on a larger study and long-term to see if the$ v A7 z7 v U4 ^$ S
response off Sprycel is sustained.
. S7 t3 ^2 l% G9 j9 y0 ]! X
: k& p: k6 W- z' d. r1 {* bBest Wishes,$ K5 V5 _! E0 A( r4 v! m$ y2 Q
Anjana9 x1 }( U4 T- D. I- n' V
/ U8 U$ e5 d6 h: h+ n3 S8 n4 k- }- o' b! [
7 t4 q- o* x4 a3 z7 Z+ L/ n/ G. m- H
Haematologica. 2011 Aug 9. [Epub ahead of print]
6 ]2 t+ o3 Y: _# n1 d/ B# q+ Q3 c: H. IDurable complete molecular remission of chronic myeloid leukemia following- ]3 W+ |6 C9 V# ~) Y+ I( S# b
dasatinib cessation, despite adverse disease features.' c3 q% ^( f2 ?/ w+ o6 R/ }
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
; w& U1 G2 I1 x$ R6 Z2 s: VSource# r: |0 X) I! i3 r! ~/ Z
Adelaide, Australia;
( M$ W, ?/ r& |! s9 A7 x3 M+ Y
h9 J) {: }' q( n* oAbstract
( Z2 A6 G2 O' B8 VPatients with chronic myeloid leukemia, treated with imatinib, who have a
h) I; a! {% Y. W0 [* H5 Y4 `durable complete molecular response might remain in CMR after stopping
6 k" Q' o$ p1 Ntreatment. Previous reports of patients stopping treatment in complete molecular
: y' l2 i7 `$ qresponse have included only patients with a good response to imatinib. We4 I9 N: s4 ^/ z2 [
describe three patients with stable complete molecular response on dasatinib1 M: _- n% S8 o/ @3 K
treatment following imatinib failure. Two of the three patients remain in I. F8 E+ T4 X$ p3 \& ]" j
complete molecular response more than 12 months after stopping dasatinib. In) F3 M# @* {* L% b1 v
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to4 `" d; @0 a+ ]0 M [
show that the leukemic clone remains detectable, as we have previously shown in
/ `- C. r, y9 L! ]" jimatinib-treated patients. Dasatinib-associated immunological phenomena, such as9 I' p9 j9 Z6 g0 k; q
the emergence of clonal T cell populations, were observed both in one patient
5 l2 o; R) @1 U3 vwho relapsed and in one patient in remission. Our results suggest that the3 C$ |+ _! W7 \5 L7 S, z
characteristics of complete molecular response on dasatinib treatment may be# y0 o: Y" d; s4 f( I
similar to that achieved with imatinib, at least in patients with adverse
9 k4 @* @$ {7 A2 ]- S4 S* odisease features.
" _1 G4 E) k1 _# `: x% Y |
显身卡
