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。* {7 i; u/ a, U8 v3 C1 `9 ~
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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作者:来自澳大利亚/ q+ i! E; o. S1 B
来源:Haematologica. 2011.8.9.
8 {, S% |. R9 Y- X7 LDear Group,
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0 Q' D7 h1 b ?! TSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML; G" f, i5 Y, x5 R8 A
therapies. Here is a report from Australia on 3 patients who went off Sprycel7 o# i, c# K1 U; Z# _* q I5 J/ D) ]
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients8 W* M; e0 J: ?# e( u- E- J
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
' j1 h2 ^/ B' t9 W6 g+ `" N* ddoes spike up the immune system so I hope more reports come out on this issue.
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b4 e0 O- J) W% P7 SThe remarkable news about Sprycel cessation is that all 3 patients had failed# o9 ?* v+ ?$ {
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
9 R! B. F* v! q, {7 N7 Cdifferent from the stopping Gleevec trial in France which only targets patients3 A8 s3 y1 n8 [+ m# N& p5 {9 N: j
who have done well on Gleevec.2 F1 d$ [" e+ N4 d
: N5 x# V/ u9 y$ YHopefully, the doctors will report on a larger study and long-term to see if the8 ^9 I. ?, o9 l2 }
response off Sprycel is sustained.
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Best Wishes,5 b$ x4 W9 P' ~. F
Anjana
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! h }/ C/ X8 J2 J" |+ q8 zHaematologica. 2011 Aug 9. [Epub ahead of print]
# H, e& c6 k( O: L4 } ODurable complete molecular remission of chronic myeloid leukemia following, V5 ~ ~* r1 x8 J0 z. m
dasatinib cessation, despite adverse disease features. Q; [# T2 E; f; Y) P
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
9 G' r9 M1 M# B# F9 QSource
3 F- x, G0 `! k% J! k, hAdelaide, Australia;
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* |$ z/ @ a7 X5 UAbstract1 z" R4 c1 I* G, M+ b( r( e9 d5 v
Patients with chronic myeloid leukemia, treated with imatinib, who have a0 \% p: Y/ ?5 x. i
durable complete molecular response might remain in CMR after stopping% D# `5 @+ X) x# ?: n3 H- `# w
treatment. Previous reports of patients stopping treatment in complete molecular
) g$ w: n+ T7 Sresponse have included only patients with a good response to imatinib. We
1 Y( P+ i' q; Mdescribe three patients with stable complete molecular response on dasatinib
* \4 K+ a8 D, k$ J" ^treatment following imatinib failure. Two of the three patients remain in) l5 A. l3 u2 I! {
complete molecular response more than 12 months after stopping dasatinib. In! ~( U5 }# J3 v+ O& C% }
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& o: y# L- ^8 I- d. |: O
show that the leukemic clone remains detectable, as we have previously shown in
9 z' d% E1 v, ~6 b3 `" W' Iimatinib-treated patients. Dasatinib-associated immunological phenomena, such as2 c6 i/ |+ T# a: v
the emergence of clonal T cell populations, were observed both in one patient t, ?7 z$ F! \, G5 h
who relapsed and in one patient in remission. Our results suggest that the
1 ?. A: h! T2 k( }0 xcharacteristics of complete molecular response on dasatinib treatment may be/ }4 k2 y# L& V4 g$ F. b3 s: O
similar to that achieved with imatinib, at least in patients with adverse+ K. m1 P/ G9 o0 I, h
disease features.& b/ s' Y' e/ Y+ X
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