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 R6 V2 y6 y6 u( Q 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。. H. q/ {9 L7 s) j) c* A) L4 m/ t
7 w- l& R7 v+ z! O作者:来自澳大利亚
* a) g+ c- f% m来源:Haematologica. 2011.8.9.7 e6 q/ C5 o8 p, i1 j) A
Dear Group,
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3 _/ V$ N6 e5 u( cSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML {" b: w7 N1 y3 \/ [
therapies. Here is a report from Australia on 3 patients who went off Sprycel
F& L% Z2 r) H1 T/ W6 y; D- Xafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients( b- P* C8 X' ^% s8 I
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
, V) C* v- y' v' O8 Ndoes spike up the immune system so I hope more reports come out on this issue.
4 M5 q$ i; w2 H! h4 d8 o+ r: z- x0 J* B, a
The remarkable news about Sprycel cessation is that all 3 patients had failed
+ o4 z% X8 d# {+ |1 h. D5 w9 AGleevec and Sprycel was their second TKI so they had resistant disease. This is
( ~7 ]2 l a7 T' tdifferent from the stopping Gleevec trial in France which only targets patients. Z8 U) V3 e) {. H
who have done well on Gleevec.* A( M8 t) Y9 d0 i4 R( }# M
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Hopefully, the doctors will report on a larger study and long-term to see if the
& h7 y2 l" T% N" t, z- kresponse off Sprycel is sustained.% P+ S( x' C7 d$ B
- D" D0 [# a2 D4 n1 }( W- IBest Wishes,
% F5 d) E. {4 F+ m# |( X% UAnjana; t1 b! z( ^- l/ Y3 y9 }
- P- g6 q+ C7 @. m* U Y) t
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! L" N' {7 f+ ^! e8 G! }Haematologica. 2011 Aug 9. [Epub ahead of print]
& o& s( D% p3 z0 V) W4 cDurable complete molecular remission of chronic myeloid leukemia following% _$ N) U; D& l/ F+ s
dasatinib cessation, despite adverse disease features." P: Q l. L: ^- b, C! d
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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% n8 J/ A4 Z" s6 ]- Q* H7 V; S7 W gAdelaide, Australia;' F3 B* u7 _9 h/ s& K
( [/ g: @; M* q" {5 WAbstract! d! e& k; A7 t4 U& y: x v E
Patients with chronic myeloid leukemia, treated with imatinib, who have a9 ~4 K: r% ^% @; }8 W6 R7 Q
durable complete molecular response might remain in CMR after stopping
9 t' m, N5 X5 z# e: {0 E; k4 vtreatment. Previous reports of patients stopping treatment in complete molecular* B) `) D9 U9 C" i4 v3 J7 D$ w) G
response have included only patients with a good response to imatinib. We- C' q( e% _6 [$ S1 v# v1 F
describe three patients with stable complete molecular response on dasatinib
* e' e3 x& ?2 Ttreatment following imatinib failure. Two of the three patients remain in
: \8 N6 c t+ T2 m5 | N% Q# u' r# u( Ocomplete molecular response more than 12 months after stopping dasatinib. In
0 r( F$ K O% x6 X' l$ Q6 J3 g* zthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
+ d# H) Z+ W0 E- ` s9 v6 \show that the leukemic clone remains detectable, as we have previously shown in! [2 U% D- s4 I6 c. }
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 X& ~; R6 y+ Q" K' k0 G6 tthe emergence of clonal T cell populations, were observed both in one patient
9 M! c$ |8 M" I- I3 Twho relapsed and in one patient in remission. Our results suggest that the' P. P& x" l2 F! ?7 W8 p6 f9 q" ]" X
characteristics of complete molecular response on dasatinib treatment may be
! Q; r2 W4 l$ V$ ysimilar to that achieved with imatinib, at least in patients with adverse
+ ], A6 c, I: r, Qdisease features.
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