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。5 v& X) i9 R' s* N4 J
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。0 x4 G. Q+ v3 E% P& h$ b
) U2 P; R/ A; t; N; e6 b作者:来自澳大利亚, R/ [2 ]" _. i2 G" K
来源:Haematologica. 2011.8.9.( A% v: u* o/ J4 q# `- S {! Z# S
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
- v" F0 l3 \& f( f7 jtherapies. Here is a report from Australia on 3 patients who went off Sprycel
) S0 V5 g, H7 o% L0 g/ hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 c/ V+ O2 j& F7 [% u" N) d" Zremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel7 x2 D) {. B/ p* I0 R" U; Y) }
does spike up the immune system so I hope more reports come out on this issue.6 F5 O& v2 N5 ~! D9 b
2 d) U8 G" R+ @+ {The remarkable news about Sprycel cessation is that all 3 patients had failed W- [; m; b5 ^: R2 s. U- c
Gleevec and Sprycel was their second TKI so they had resistant disease. This is% y$ m: y* t# T: J4 s; y+ t' i# Z
different from the stopping Gleevec trial in France which only targets patients
4 B, x! ~( r c5 o Z2 U& Ywho have done well on Gleevec.
e+ h! J4 @$ F4 Y8 ]
$ l8 @! T, d3 `" z T9 oHopefully, the doctors will report on a larger study and long-term to see if the3 N a1 q9 }* ?! d! S; G
response off Sprycel is sustained.
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Best Wishes,+ L- d; A- @& _/ v9 z7 ?; Y
Anjana
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! `: u4 v3 q# R/ V/ E- ?, Q+ e, y0 D' S3 {
, ]1 @/ I* M5 P( ?/ w* H% oHaematologica. 2011 Aug 9. [Epub ahead of print]
' J( a! }. x4 C, \Durable complete molecular remission of chronic myeloid leukemia following
$ J2 q+ e& v4 C; |: T3 n% A ldasatinib cessation, despite adverse disease features.3 E3 B. J9 x, `
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
) M" x- U+ F" x) ]Source
7 [: s. K0 J2 R8 C4 d, I' f/ n( f8 WAdelaide, Australia;
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3 T) P1 L/ p: C) g; l3 qAbstract6 g c( P l6 q
Patients with chronic myeloid leukemia, treated with imatinib, who have a
0 k3 C( U/ {: {: w8 Q5 k: ?- Ddurable complete molecular response might remain in CMR after stopping& Q8 c# g J" y( T; m" H
treatment. Previous reports of patients stopping treatment in complete molecular
+ V) ^$ N1 @# x! {* N) h" Vresponse have included only patients with a good response to imatinib. We
5 q9 [& y& H! G+ idescribe three patients with stable complete molecular response on dasatinib y2 j# A2 |- r
treatment following imatinib failure. Two of the three patients remain in
, N- o! \6 g# ^0 v6 ^ fcomplete molecular response more than 12 months after stopping dasatinib. In
; i2 F6 \) }. d2 h) tthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
0 m! u& w* ? V( Z' f% wshow that the leukemic clone remains detectable, as we have previously shown in
9 X/ F$ j) g! u5 p3 nimatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 f0 h: i: F4 P5 R Q# A: t
the emergence of clonal T cell populations, were observed both in one patient) x/ @" N: P( ^ w+ {0 O4 m5 p
who relapsed and in one patient in remission. Our results suggest that the
7 D( b$ z# h% E+ @. Q' L- tcharacteristics of complete molecular response on dasatinib treatment may be Z* ~$ K. x) O* Q8 S% Z0 B
similar to that achieved with imatinib, at least in patients with adverse
& e6 x9 c; X9 x7 s& ^' C: edisease features.7 g& I" h/ Z0 c9 z: U% `# M3 ^# B8 y
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