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。! u) S j6 z+ y8 ~, @0 X
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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! s+ y5 t5 L: u3 [' v$ J. d8 s6 T作者:来自澳大利亚
" O3 m; z0 h; G! x3 M! f来源:Haematologica. 2011.8.9.& X3 C v$ X0 d! M% A
Dear Group,# J$ [6 ^5 G2 [" S" l
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML) [/ m% K6 N X; @2 \) e
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 v- g1 y* z/ @. c5 q: R, b
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients! K R! b6 ?- N) G* B5 [9 h
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel+ p& [6 f8 V2 S4 `) {. B* d
does spike up the immune system so I hope more reports come out on this issue.
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$ `, v* q' P; m7 z8 r1 Y4 o# E KThe remarkable news about Sprycel cessation is that all 3 patients had failed3 S! X. C, k! n7 D, \9 ]. R
Gleevec and Sprycel was their second TKI so they had resistant disease. This is/ p: b2 R. ^( Y0 y
different from the stopping Gleevec trial in France which only targets patients
3 E9 M. ]( Y3 F, r4 twho have done well on Gleevec.
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7 h9 H3 ~8 I/ I( {, [& DHopefully, the doctors will report on a larger study and long-term to see if the
N" I" [+ y! P. @8 vresponse off Sprycel is sustained.
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# m; n6 m1 g. J, e% O( @# c( uBest Wishes,% R$ Z! |3 |# Y+ c: ^0 P, E
Anjana( a$ a/ x6 G. ?' d) @
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+ M% A% d# s+ ?& | yHaematologica. 2011 Aug 9. [Epub ahead of print]5 v8 `, T/ o) P/ B* B7 ~- a' c
Durable complete molecular remission of chronic myeloid leukemia following8 F0 {9 [& S2 {! O; y0 z* h
dasatinib cessation, despite adverse disease features.
' r7 F( v+ ]8 G$ DRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.! r5 _0 X. b2 G6 k- C0 _
Source9 {* J8 i" `, H1 \
Adelaide, Australia;: K, J8 C5 y6 v" q i; d+ L( M
3 V* d4 `& d5 X* K8 J! dAbstract; z6 d! P! L& m( {
Patients with chronic myeloid leukemia, treated with imatinib, who have a9 G' c; a+ k. H- h: c. F: q" c
durable complete molecular response might remain in CMR after stopping( b; X6 G. ~- w, k$ |; p
treatment. Previous reports of patients stopping treatment in complete molecular
# N( @7 t9 `) M" i: l9 T/ S! o; T7 V+ jresponse have included only patients with a good response to imatinib. We/ V4 x: J/ S7 e: `( K
describe three patients with stable complete molecular response on dasatinib8 L3 v& t) A( q8 h5 x/ g
treatment following imatinib failure. Two of the three patients remain in& K4 c5 \: V- j7 K' W- C) p N
complete molecular response more than 12 months after stopping dasatinib. In
- b! x) u* y' |/ t8 L" Sthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to z2 n, G' [0 o3 l
show that the leukemic clone remains detectable, as we have previously shown in1 C, T3 h; p- Q V9 p C8 e
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
- |# K" X4 {9 Nthe emergence of clonal T cell populations, were observed both in one patient
7 H: k5 c7 M$ Y5 Y- Y, d2 U9 gwho relapsed and in one patient in remission. Our results suggest that the
2 F* J0 t- o( `5 W' ycharacteristics of complete molecular response on dasatinib treatment may be1 d5 f2 d5 S+ f' y' A0 S
similar to that achieved with imatinib, at least in patients with adverse
4 j" i' t4 E% C7 g- Rdisease features.
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