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。( o; d2 s# E& R$ c7 \8 [4 H( k4 r( a
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。7 }7 ~; k7 R8 S" t
4 Z v2 I- J* m7 d+ A4 R作者:来自澳大利亚, g2 W X" {+ d
来源:Haematologica. 2011.8.9.+ u2 o7 n" V s+ f) ]1 h3 Z
Dear Group," b7 z1 O0 F$ K) o: f, F: S
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML9 B6 c5 u# [, p8 O; E4 q
therapies. Here is a report from Australia on 3 patients who went off Sprycel
+ X4 g- c- }- E7 cafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
/ t# H4 B) c% b5 l" oremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 a0 J) k7 F$ J* r! _8 W' O, O E7 [
does spike up the immune system so I hope more reports come out on this issue.6 H5 C y0 Z0 F' j% [- M
7 r3 h, `; ?6 d: g% ?
The remarkable news about Sprycel cessation is that all 3 patients had failed4 B" T; g9 F0 e6 z6 H
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
+ h& e/ F9 |5 h. F/ D! kdifferent from the stopping Gleevec trial in France which only targets patients3 \6 V9 n! N% r3 c
who have done well on Gleevec.6 P3 z, P; B1 @' S C$ S7 L
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Hopefully, the doctors will report on a larger study and long-term to see if the5 ~% `5 [2 Q( }) U, K+ o u- |
response off Sprycel is sustained.+ Q' M% s8 p8 J. T6 U/ @
2 [: t/ v; |2 a- b0 zBest Wishes,$ O7 F V$ f4 f3 B# T! B
Anjana U4 o+ P0 k; K! @
2 s% i) k/ V7 E
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Haematologica. 2011 Aug 9. [Epub ahead of print]
- L' H4 ^7 a% J! X% m3 oDurable complete molecular remission of chronic myeloid leukemia following' s6 I/ Y: d8 G9 [% e
dasatinib cessation, despite adverse disease features.
1 a5 V4 ]3 D; ?2 y/ E" HRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP. K3 m1 X1 f- s0 i( C
Source
6 \+ f! T' U0 G" a KAdelaide, Australia;
6 {) k8 |& ?! h# i4 D; U( ]; f" o; Y* V- D% ~1 @ Y9 V
Abstract
: `3 C2 B% Z& ~5 k. q8 Y5 I6 M8 XPatients with chronic myeloid leukemia, treated with imatinib, who have a
5 E4 A* z5 X d8 n% Y, ?: {7 }; ndurable complete molecular response might remain in CMR after stopping
1 Q! p* K& k c7 ]$ K4 _( Itreatment. Previous reports of patients stopping treatment in complete molecular
% Y6 i% q% T2 b5 T/ Y6 d/ [response have included only patients with a good response to imatinib. We
8 U# X4 z3 v% H* @0 a k) O4 Sdescribe three patients with stable complete molecular response on dasatinib9 s. ]4 Y) t" w% M! F9 X9 ~" k
treatment following imatinib failure. Two of the three patients remain in4 t* v0 q% [- L. S: R# s
complete molecular response more than 12 months after stopping dasatinib. In* s" Z' q+ K2 a( t
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to( @+ M+ a/ D9 G) \/ I* W- [
show that the leukemic clone remains detectable, as we have previously shown in" d3 U. y% j( S( Z9 n P3 Y9 ~
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 J2 G ?3 L- V& S
the emergence of clonal T cell populations, were observed both in one patient
$ Z" J* g& s7 s( `1 S0 ~who relapsed and in one patient in remission. Our results suggest that the9 A8 Z7 ], y. ?* [
characteristics of complete molecular response on dasatinib treatment may be
( w$ {9 W& ]" \% [similar to that achieved with imatinib, at least in patients with adverse
1 S$ m+ ~4 A; L U8 qdisease features.: l- a) {1 i {0 o5 d+ k
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