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 w+ X. B+ Q# K 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。5 L C5 y L, u$ f# o
; ?/ D' A( B' D作者:来自澳大利亚
) q, H `5 t/ q( M8 }来源:Haematologica. 2011.8.9.' \' ]* P; B/ t1 e; v0 f2 h( O4 G* E
Dear Group,$ U- Q( o6 i- p, a7 l
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML2 e6 h# q- i, X9 j3 ?% E( s; R
therapies. Here is a report from Australia on 3 patients who went off Sprycel
3 w+ G) l) A5 H( W% S( H4 f$ u1 yafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients! ~8 @0 T* f; `7 A! ^$ b$ ?
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. F9 R" j* s, c/ g
does spike up the immune system so I hope more reports come out on this issue.
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3 v0 W$ X% ?' b4 y/ kThe remarkable news about Sprycel cessation is that all 3 patients had failed
; l' C) x8 z6 \% H$ VGleevec and Sprycel was their second TKI so they had resistant disease. This is
* O: y) ~' g+ K8 _/ \different from the stopping Gleevec trial in France which only targets patients7 ^+ W% m/ j" v3 i0 [
who have done well on Gleevec.
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$ p4 h b/ _7 b* j) H4 ^* CHopefully, the doctors will report on a larger study and long-term to see if the' F( G! W; t) s
response off Sprycel is sustained.
6 i8 Z# b `2 G
4 ~7 ~) |! c+ _8 h* ~3 E! \Best Wishes,
8 K6 y/ o' @1 LAnjana
1 b9 ^' L" \7 |0 d/ I9 i; y$ ]
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8 D- f3 q1 V7 S+ B2 V+ @1 A$ J ? o) z. W' m* X
Haematologica. 2011 Aug 9. [Epub ahead of print]% a% n: |3 H. S. g
Durable complete molecular remission of chronic myeloid leukemia following8 `+ R7 }) x c1 z0 [
dasatinib cessation, despite adverse disease features.
' r$ j8 p3 |6 o9 B5 kRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
7 v( G+ J4 t: s# J( w$ CSource
9 V5 a: Y4 w( A( \. a) h. zAdelaide, Australia;; z3 j/ n' x1 |, R
& |2 b* ^6 i( n% b: M/ V& I4 x% X
Abstract2 \: [ I5 l( `9 P0 o$ v
Patients with chronic myeloid leukemia, treated with imatinib, who have a
( j4 @+ d! D0 g2 J5 Y7 I3 `durable complete molecular response might remain in CMR after stopping
8 \0 ~8 k* Z e/ Htreatment. Previous reports of patients stopping treatment in complete molecular
/ r n$ `+ b' D7 Gresponse have included only patients with a good response to imatinib. We
! C/ H& p. Z; |0 B& D. K ldescribe three patients with stable complete molecular response on dasatinib. X6 x( L, Z" y8 h9 q) {
treatment following imatinib failure. Two of the three patients remain in
) R& g9 _; ?$ y- e5 xcomplete molecular response more than 12 months after stopping dasatinib. In1 t6 M% r/ g7 s$ S5 E
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to N; [0 y& Y. l" ~! w
show that the leukemic clone remains detectable, as we have previously shown in
. r& k9 G" X4 K9 r0 Nimatinib-treated patients. Dasatinib-associated immunological phenomena, such as3 z7 X. G# f z: ~' H) J9 o
the emergence of clonal T cell populations, were observed both in one patient0 H: ~/ }% a3 ^2 P: k0 v
who relapsed and in one patient in remission. Our results suggest that the% K1 d0 D8 M5 q% n( V2 U3 N
characteristics of complete molecular response on dasatinib treatment may be
) J& E4 f8 `5 f3 \$ m3 O8 x# {. Isimilar to that achieved with imatinib, at least in patients with adverse
0 L T/ n: U: F8 @& fdisease features.
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