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 V$ u3 C! O6 @
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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! q, O" @7 H# P作者:来自澳大利亚
' `: ^8 L( M h2 H, x; p+ x `1 b来源:Haematologica. 2011.8.9.5 N9 K0 a2 Y8 q( w) P3 q: _$ V
Dear Group,3 p) g @7 W0 o9 n% a5 ~
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML7 w5 C) G+ J2 o3 w, K8 h) F! t
therapies. Here is a report from Australia on 3 patients who went off Sprycel
# ?; e6 x% v3 b. eafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
y1 M& ? s6 p/ tremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
' C) }1 c9 S$ L; Xdoes spike up the immune system so I hope more reports come out on this issue.
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4 I! q3 X1 @* aThe remarkable news about Sprycel cessation is that all 3 patients had failed
1 N# L2 E, \# U/ JGleevec and Sprycel was their second TKI so they had resistant disease. This is
* Z0 Q" l g; B1 d5 Y0 gdifferent from the stopping Gleevec trial in France which only targets patients
: G; o2 K' w( _2 A9 G: v$ U, Gwho 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
5 j( S; ]+ t& T @response off Sprycel is sustained.: y, b" v# B5 u0 |8 b( t0 Z; q
u8 E0 W/ J9 g/ E) [& Q: n7 f
Best Wishes,
& S' {. D4 e& F/ I5 W! RAnjana4 a/ d% L" Y- @5 F$ ^# P9 [
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, W) ~0 g' j% u5 l) Q. mHaematologica. 2011 Aug 9. [Epub ahead of print]( f* D6 q! U/ v8 ?. ~/ g
Durable complete molecular remission of chronic myeloid leukemia following
7 P8 {( `* [. Y' O* Hdasatinib cessation, despite adverse disease features.' b; U7 f6 y/ v5 u! z" w3 s
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
+ b5 ~2 v7 L# d6 _9 `/ @& h- h; YSource; {- W9 |* g+ i' m7 {8 r$ O
Adelaide, Australia;
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Abstract- \/ ~- S. s, s9 Y- f/ E! h
Patients with chronic myeloid leukemia, treated with imatinib, who have a$ p! {5 h M$ O
durable complete molecular response might remain in CMR after stopping8 O& [. O3 D9 X4 O, V
treatment. Previous reports of patients stopping treatment in complete molecular# m' o" O, \5 W" x3 n
response have included only patients with a good response to imatinib. We
i# Y$ g% m; B8 p+ Y; V7 d' Vdescribe three patients with stable complete molecular response on dasatinib( U, \- Y5 `) v# g/ z: m' X. r
treatment following imatinib failure. Two of the three patients remain in! E, O, B4 R$ B/ j. W
complete molecular response more than 12 months after stopping dasatinib. In& A7 [: c. [# H" j8 s; j
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
# ?9 D; u Y+ R$ w, D5 b' s8 eshow that the leukemic clone remains detectable, as we have previously shown in
4 L* W9 F, ]# {+ I1 @( simatinib-treated patients. Dasatinib-associated immunological phenomena, such as! p1 e; F' T# x
the emergence of clonal T cell populations, were observed both in one patient
8 b( @' j# U p: W6 h7 P& Jwho relapsed and in one patient in remission. Our results suggest that the; r u* _9 b/ U' m/ W
characteristics of complete molecular response on dasatinib treatment may be
9 s( J6 ?, T. v" e3 f. Lsimilar to that achieved with imatinib, at least in patients with adverse0 U2 Q* T4 ?3 \/ O6 u( K- I
disease features.
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