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。
6 Z2 c$ h( V1 z3 F2 ] 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。" {( P0 f, N$ t: V8 M
7 \) ` x$ N+ a# z: d作者:来自澳大利亚. @6 a' T- S1 |$ W. m: I6 G
来源:Haematologica. 2011.8.9.
/ T8 R7 M+ X1 q4 u3 K5 L& u; r% cDear Group,5 e' F# J9 h4 b2 p- F
( H; |" ~1 C( B5 hSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
4 T) C9 p$ l& {9 _( E) Ltherapies. Here is a report from Australia on 3 patients who went off Sprycel
" ~- }$ W2 b# y, ?5 T! L/ H5 B* `after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients( u4 B7 T0 V, B" d8 I
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& K. H* o1 C# sdoes spike up the immune system so I hope more reports come out on this issue.: ?2 j G# \/ Q* e& P8 i
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The remarkable news about Sprycel cessation is that all 3 patients had failed
) k& E- k& J' T9 n! o: jGleevec and Sprycel was their second TKI so they had resistant disease. This is
. N$ f+ r6 n8 W$ i3 ^0 H% ydifferent from the stopping Gleevec trial in France which only targets patients: o6 D. D6 \. z. \$ {
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the( T* s. ]3 V0 |# ~* V- r3 c% C
response off Sprycel is sustained.
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Best Wishes,
' V4 f8 T) n1 n$ D" }8 JAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]; H# S! j0 y+ m, ^
Durable complete molecular remission of chronic myeloid leukemia following
: |/ c; v$ ^( P! ]9 |dasatinib cessation, despite adverse disease features.; z. f- w3 L* N6 T
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.) A/ K- k) ?( f
Source
$ G) B) m+ F: y! C$ k8 q* hAdelaide, Australia;/ k( x0 F2 J" `
+ q; x0 o4 `: [! Y# [; X6 O
Abstract
% a! s6 k) c$ t% S" ?+ z" _Patients with chronic myeloid leukemia, treated with imatinib, who have a
4 g# i5 D8 A; |5 L, T& F/ Rdurable complete molecular response might remain in CMR after stopping$ r3 o6 d+ U/ W2 c
treatment. Previous reports of patients stopping treatment in complete molecular
' Q2 J4 P4 V! n% e2 e0 V% ^: Bresponse have included only patients with a good response to imatinib. We
* P+ s, o2 D% ]1 M, K: l: rdescribe three patients with stable complete molecular response on dasatinib2 C. k) a5 p$ a3 y
treatment following imatinib failure. Two of the three patients remain in6 B! s& w/ E- t: G5 O' ]$ q
complete molecular response more than 12 months after stopping dasatinib. In) X# l3 K p9 S/ J3 l; C
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to. e9 A+ g. L+ u0 D
show that the leukemic clone remains detectable, as we have previously shown in+ b4 {, T# [/ i& @; [0 k' l* p
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
( `9 p' [$ k' U; @+ Jthe emergence of clonal T cell populations, were observed both in one patient8 I2 }/ a- R5 R% Y/ {7 d; f
who relapsed and in one patient in remission. Our results suggest that the
! P0 @; p0 k* K! P+ o6 Ccharacteristics of complete molecular response on dasatinib treatment may be% _: \2 e* |% x; C6 o9 ]
similar to that achieved with imatinib, at least in patients with adverse) P/ v+ ]$ g" x: v' I
disease features.9 n* H6 T i: W* [: s) E
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