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 `8 g) E# ~8 P, r& S3 x
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 t( m3 r/ u, F/ E8 M# L+ B6 K
" Z+ o2 T. ~& [! R6 w9 `# X3 A: z$ J" g, u作者：来自澳大利亚
, R/ d8 |: N; j {, t$ L: ?9 @来源：Haematologica. 2011.8.9.
' E+ t# @ c1 K9 n. [4 u& ]( lDear Group,2 J; T5 H* ?# X( P3 f$ s# n# u1 a
/ J: ?* D2 I6 T: q7 w( ?& e
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
% I& z9 B7 I6 `therapies. Here is a report from Australia on 3 patients who went off Sprycel
* @9 J4 ?0 X" g/ A; g: Kafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
3 i$ [/ t5 P- }remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel, E( s& e$ a1 q3 j, @' K" P$ S5 o% q
does spike up the immune system so I hope more reports come out on this issue.
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6 A. i& N. D1 b; l& hThe remarkable news about Sprycel cessation is that all 3 patients had failed
5 d9 R! G# t% aGleevec and Sprycel was their second TKI so they had resistant disease. This is
4 G" @$ G! j2 B9 Wdifferent from the stopping Gleevec trial in France which only targets patients3 {' ~1 s6 D' Q% U& S) l
who have done well on Gleevec.; ]# r- x( i2 F8 e; E
! f# d, a) T0 `( ~: @! iHopefully, the doctors will report on a larger study and long-term to see if the+ i- G! I7 l1 H5 m$ y
response off Sprycel is sustained.
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9 }2 t; y, |+ W0 U6 uBest Wishes,5 Z8 f. g- \( v" z+ j& v, X& e" w( ^: ~
Anjana
, @' u7 q3 U# D8 f* d& w2 b2 f g
% T* H0 S; c* t& z- O; w# Q$ F! o T2 w& a3 [+ e8 i$ A
+ K* F5 I# s8 ]6 b5 H3 pHaematologica. 2011 Aug 9. [Epub ahead of print]
5 G( R6 t! Y# r& b: IDurable complete molecular remission of chronic myeloid leukemia following& w5 X$ E, }- R" ^
dasatinib cessation, despite adverse disease features.3 v2 T# N9 g) Q1 y* f; N M0 v
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.3 c2 L6 @+ \( f9 y z# b8 S) \
Source: [0 S6 w* k, g3 \3 T6 e1 }! R: W9 u" j
Adelaide, Australia;: Y5 l/ k; ~. ~0 l
* ~6 V# ^' z/ C, o* OAbstract
4 h" ^& h& h5 R$ GPatients with chronic myeloid leukemia, treated with imatinib, who have a
2 ?1 j9 c v+ R, vdurable complete molecular response might remain in CMR after stopping
* p# s+ w; J' Ntreatment. Previous reports of patients stopping treatment in complete molecular
* K5 \8 S2 p; N3 a3 U hresponse have included only patients with a good response to imatinib. We4 G, v* F4 ~- K" u% v/ X9 ~
describe three patients with stable complete molecular response on dasatinib
3 B0 |* Z+ c2 e6 [: _treatment following imatinib failure. Two of the three patients remain in- U+ T. C) [3 M1 P4 |% [$ O0 {
complete molecular response more than 12 months after stopping dasatinib. In1 h3 d7 i) T$ q9 {$ |: ]$ Y
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, F1 E1 A3 a4 w2 }
show that the leukemic clone remains detectable, as we have previously shown in3 Y* T x, S4 N" X; m
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as3 k- _, f. p% d" F" g3 y" g* ^5 Q* m
the emergence of clonal T cell populations, were observed both in one patient$ t( Z6 J; V+ S1 \# W3 x
who relapsed and in one patient in remission. Our results suggest that the& f* j) e) Y3 H N: b+ y( h; `
characteristics of complete molecular response on dasatinib treatment may be
7 r7 m7 K$ H$ Z7 x: k1 f" D7 M8 m, Isimilar to that achieved with imatinib, at least in patients with adverse4 k" c" S2 @0 O0 M& Z# h
disease features.
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