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。
' v( h/ Q ~! F a l 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 ~3 V6 Z, {. k1 a: D作者:来自澳大利亚
& k& q/ ~0 @, S. Z% R来源:Haematologica. 2011.8.9.
7 A/ d8 } M3 x+ D" KDear Group,
Z8 @& ^6 ^' v h; \; K% M0 A% s2 A- W4 G7 h
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
- l6 d: C) m8 A7 `3 O% ttherapies. Here is a report from Australia on 3 patients who went off Sprycel* a& a# m5 Y. ^
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients6 t' G1 N0 `5 b- o( T2 h2 {) k
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel6 D# P0 I0 i8 E M
does spike up the immune system so I hope more reports come out on this issue.
9 ^% a% S# X. _, m: l% l: M# K% z: ^. e w( g7 t5 }- f
The remarkable news about Sprycel cessation is that all 3 patients had failed9 _( x6 m7 x* a) V& e, E }7 _
Gleevec and Sprycel was their second TKI so they had resistant disease. This is i" X0 \0 [+ o8 l
different from the stopping Gleevec trial in France which only targets patients
* d9 n( U' |) S6 Nwho have done well on Gleevec.
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4 [1 e: Y) P# h4 x1 } T6 pHopefully, the doctors will report on a larger study and long-term to see if the
, A( Z t7 k# J( U9 s) Bresponse off Sprycel is sustained.
+ ^+ w8 W$ P0 g9 C$ I, o
7 A' e2 l, E6 L* y8 {) xBest Wishes,
. Z+ E7 ]- j% Q3 hAnjana2 n. A1 [% Z" B0 f9 P
6 H! I. \( e$ ~- g8 u7 ^7 q
- D" a# M9 o s- h0 W3 n% R# Y
4 f5 L' d; L' p$ B2 k5 ^+ vHaematologica. 2011 Aug 9. [Epub ahead of print]
+ C; p5 G0 v6 j, e7 `$ HDurable complete molecular remission of chronic myeloid leukemia following
& m! L6 b( T2 {% D6 R: Ldasatinib cessation, despite adverse disease features.
3 N( m: u& R, \2 ~+ IRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.3 r* s% q H; t f0 A
Source2 O1 W' F* M! V* w5 z
Adelaide, Australia;
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4 i9 Q" J, U4 b, p. O$ FAbstract
3 a1 B. X& n+ DPatients with chronic myeloid leukemia, treated with imatinib, who have a
) F$ ^4 W3 i; c* W8 W- pdurable complete molecular response might remain in CMR after stopping6 l. E8 o4 q* W0 o. q9 J* e K8 d& Y
treatment. Previous reports of patients stopping treatment in complete molecular
$ s' k$ E+ K# A6 f5 p$ u3 W$ eresponse have included only patients with a good response to imatinib. We
. T e3 [/ F- b5 ]describe three patients with stable complete molecular response on dasatinib
2 T5 u2 Y$ G1 d; w* Q3 Z' ytreatment following imatinib failure. Two of the three patients remain in: b e" c+ [/ _& M/ A0 O5 T
complete molecular response more than 12 months after stopping dasatinib. In
% P9 H. S: ~+ b- h/ d; ythese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
+ X2 o1 V; b$ Y$ k5 b$ D" z7 A& c' Ishow that the leukemic clone remains detectable, as we have previously shown in# o0 s4 W1 G) |1 y7 J
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 R' R/ M, G2 ?2 Z! v4 ythe emergence of clonal T cell populations, were observed both in one patient
4 ? x3 z6 R5 o7 Z+ d" _0 e# W: k0 dwho relapsed and in one patient in remission. Our results suggest that the7 T% U+ N' l$ D& e2 v! D3 [- Y! A
characteristics of complete molecular response on dasatinib treatment may be g# n7 }# h- w! ]
similar to that achieved with imatinib, at least in patients with adverse
/ H- h' [' {- y' N ~disease features./ _2 y5 b; C4 V. o4 Z/ E
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