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。! r) Y) \1 p5 D
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 o8 b: b+ {) C( j5 i: g+ e
. a" z; F* Z" {8 U) w6 k# r作者:来自澳大利亚
2 s7 }8 H6 l2 C7 r5 C7 K来源:Haematologica. 2011.8.9.
. _, t* I! b. J: }5 FDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
2 V) k% ^/ h# ~/ | Vtherapies. Here is a report from Australia on 3 patients who went off Sprycel
8 k w" ]! f! }+ M) Oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients$ O5 l. G! k/ S8 f% L$ W
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
4 m# w: W4 |" c0 I$ C/ wdoes spike up the immune system so I hope more reports come out on this issue.$ Y+ ?$ @( x! T6 d* @- |
3 {( [( A9 Q9 o" FThe remarkable news about Sprycel cessation is that all 3 patients had failed
% o6 x5 s* M4 ^4 l: A( H3 BGleevec and Sprycel was their second TKI so they had resistant disease. This is' w: p. d4 M% k' J/ f8 l& M
different from the stopping Gleevec trial in France which only targets patients
) A4 z( p* `& W. N% N5 L4 E. bwho have done well on Gleevec.
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4 ^0 M; t' z: X# _* \7 ]0 hHopefully, the doctors will report on a larger study and long-term to see if the
! g9 Y$ q3 f0 i0 ]1 X+ presponse off Sprycel is sustained.
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. M' u. x% e2 N2 }6 G1 N5 n( vBest Wishes,
+ U- q, U1 J3 m! b% m- w) z* eAnjana
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# M g1 o8 v/ C" h* [- {Haematologica. 2011 Aug 9. [Epub ahead of print]% A( k7 v: v, h* y L
Durable complete molecular remission of chronic myeloid leukemia following
* y; P' h4 i$ Q2 n i4 q1 o% @dasatinib cessation, despite adverse disease features.
J2 `% a% ]' `" a2 m' G4 iRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ }0 ~" K% v, g& W% O* C
Source
7 q* q$ G# `2 YAdelaide, Australia;; m, c# U1 Q4 g& p' L$ [
7 W/ y% L+ B7 k# H/ H9 `7 L
Abstract3 E* O$ c) {( w$ r; ]& m4 I5 D9 I
Patients with chronic myeloid leukemia, treated with imatinib, who have a
. s& V, X4 ~' w |) L a7 Z. Xdurable complete molecular response might remain in CMR after stopping
+ P F7 I" L8 c% D% Gtreatment. Previous reports of patients stopping treatment in complete molecular8 r) ?. v' p/ c a# K
response have included only patients with a good response to imatinib. We
/ n9 ~. ~" L! q8 m; s4 ~4 Cdescribe three patients with stable complete molecular response on dasatinib
3 `7 R5 ]( |5 ktreatment following imatinib failure. Two of the three patients remain in
( E" D1 T* j5 U* H! |7 l3 dcomplete molecular response more than 12 months after stopping dasatinib. In0 }. M: R% f+ H( o0 T
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& c4 t2 \; g; K: F1 H
show that the leukemic clone remains detectable, as we have previously shown in! M. m' d- h; Q) H0 a
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as. G2 r; D- A2 Y+ @: S" x7 s
the emergence of clonal T cell populations, were observed both in one patient C' C7 V* r- G7 y% _
who relapsed and in one patient in remission. Our results suggest that the
& Q1 K7 {( {. Y }, A* q+ Wcharacteristics of complete molecular response on dasatinib treatment may be- f" F; Y$ d/ d1 p. @
similar to that achieved with imatinib, at least in patients with adverse
8 D* ?/ i5 }0 x% r. v/ `' ~disease features.# w0 h# s6 x$ e% L
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