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。
$ \# b( a9 ]! ~9 N. _& N 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。
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7 h" j) a" b6 y作者:来自澳大利亚 i5 r/ l% m9 _4 U& `2 c$ j# k2 B! e
来源:Haematologica. 2011.8.9.; J Y' |% A- O5 m. j
Dear Group,, b) i# j% P/ O6 U
8 F: F- o7 w! r0 {( j! p
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML' \9 d9 n ?" F- Y' @6 F
therapies. Here is a report from Australia on 3 patients who went off Sprycel
3 z f( A. ~ R e- oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ R& e8 l/ k6 r$ C" a5 rremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
9 R" I E/ e7 }: a$ i" Wdoes spike up the immune system so I hope more reports come out on this issue.6 D% S: a! ]7 z w
% ?* `* [ p. n$ ^% U! e2 iThe remarkable news about Sprycel cessation is that all 3 patients had failed
5 O; J: P: E% M1 }( {1 P6 G$ k. bGleevec and Sprycel was their second TKI so they had resistant disease. This is
, X/ j( V) {1 k# xdifferent from the stopping Gleevec trial in France which only targets patients
/ @$ d( i) _2 v& Z1 Z( g9 @who have done well on Gleevec.5 |7 ^4 U9 m, F( _2 B9 j# A2 M
+ ~3 l) O( n( R9 g, }: V
Hopefully, the doctors will report on a larger study and long-term to see if the
! v: u" \9 e* y2 J3 X+ C0 q$ ?response off Sprycel is sustained.' N+ H( S! q- a& F& Q& X l
# U: G) F A' d3 r
Best Wishes,
9 g4 j9 {/ U: u* M/ ] V q% J' aAnjana* S0 g; O" e# b3 [
4 ]* L* Q f/ w' g
7 q7 B) n0 \- [% w: O( ] d& M5 I# A- U) g, [3 a- [
Haematologica. 2011 Aug 9. [Epub ahead of print], @1 J( u; a4 X9 v
Durable complete molecular remission of chronic myeloid leukemia following
, N- e: `, c# N& W8 Q4 _1 H4 Bdasatinib cessation, despite adverse disease features.: x7 u" o! o& n; q c- `+ r+ f- J) P8 U
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' S- F2 f6 ?3 N0 N: X# c! q( c& F
Source% L# z* @% L4 R L% g
Adelaide, Australia;2 x; n, C, b+ h: |+ X- f
/ n2 C. C0 k u1 JAbstract
9 R1 L) |& | g v5 K/ ` ^Patients with chronic myeloid leukemia, treated with imatinib, who have a
7 a/ k5 Q, h0 b3 ^1 Kdurable complete molecular response might remain in CMR after stopping
- |5 ?0 c) Z: X! b ^, l% m2 n xtreatment. Previous reports of patients stopping treatment in complete molecular& F4 H! A( l9 s5 O& o r
response have included only patients with a good response to imatinib. We9 Y6 q9 m0 T4 e N9 X1 J% a5 F0 A9 i
describe three patients with stable complete molecular response on dasatinib
+ N2 M/ I9 u% X0 n/ ~( c5 V8 M8 gtreatment following imatinib failure. Two of the three patients remain in* x- E% W, P1 P, d# E
complete molecular response more than 12 months after stopping dasatinib. In
+ v, i' K8 \$ T, J5 C- w, wthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' I' N: X! l0 y+ w H, Z# I8 L: ?show that the leukemic clone remains detectable, as we have previously shown in
' d, b2 b) S; F- G7 s! i& rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
; Q+ I& a0 P6 K; T3 Z5 Jthe emergence of clonal T cell populations, were observed both in one patient
* _% l; N: k* b# \who relapsed and in one patient in remission. Our results suggest that the5 X( v7 [& G! B+ o
characteristics of complete molecular response on dasatinib treatment may be. b* ^ a6 k5 M% N7 f
similar to that achieved with imatinib, at least in patients with adverse% B H. ]# E( R' o* q" b) T: F
disease features.2 l! }9 T2 W# @+ q1 ~ _$ V$ b0 Z
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