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。
. K: g; E0 |3 k! }9 A) v) I 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。: S2 [* m: O9 k/ M" Z( s7 Z, P
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作者:来自澳大利亚
0 P0 Y! Z0 K$ h来源:Haematologica. 2011.8.9.& H# W5 H% W! Z
Dear Group,
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8 ]. I' v! F f9 Z% m; e' DSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML0 j& I$ `; t% n A0 r& A9 |2 @1 v% c
therapies. Here is a report from Australia on 3 patients who went off Sprycel& O N% ^! T+ E! O, n! Z7 o1 b
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, N. }* W& W$ t+ K. fremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel: q4 X# X2 V2 u* a. U/ b
does spike up the immune system so I hope more reports come out on this issue.
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4 y$ R8 Z% |3 F4 GThe remarkable news about Sprycel cessation is that all 3 patients had failed" U; K9 F" {/ c. m
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
R" S" m$ _9 v* udifferent from the stopping Gleevec trial in France which only targets patients. O6 }7 [5 y3 k1 x, L$ d I; V
who have done well on Gleevec.7 ?- Y; m4 e: r- D3 S
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Hopefully, the doctors will report on a larger study and long-term to see if the
8 B+ w& h, N: D; A$ Sresponse off Sprycel is sustained.
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2 p, I. q) J) tBest Wishes,
: F: t) Y8 y% v5 _ z3 MAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]1 V# w4 W- s c. O8 `5 p' k' T5 d
Durable complete molecular remission of chronic myeloid leukemia following2 F8 R/ H0 {4 v" ~# P! I! t P) z
dasatinib cessation, despite adverse disease features.: ` h' b1 X# M6 u7 B
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
6 G2 a+ R1 W, I* B# `2 d1 zSource
2 t7 E: d' ^; P. R0 U5 SAdelaide, Australia;9 U1 _! {3 J% U
) r. \- k; h$ C: c5 D6 HAbstract
+ B C0 i" M+ D J' KPatients with chronic myeloid leukemia, treated with imatinib, who have a
_+ m8 Y4 {* b7 `# H1 Odurable complete molecular response might remain in CMR after stopping
1 p5 N' L; W8 @3 d2 ?treatment. Previous reports of patients stopping treatment in complete molecular) d, B ^6 N: |; f4 y ^0 |. A
response have included only patients with a good response to imatinib. We
, m/ o$ q$ e9 O; Mdescribe three patients with stable complete molecular response on dasatinib: \3 M; u" q$ u
treatment following imatinib failure. Two of the three patients remain in
- v0 w( v7 h7 x. n0 f3 N6 Z, bcomplete molecular response more than 12 months after stopping dasatinib. In Q$ K$ N, q& ?6 G6 b
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' Z5 F- v+ `; c( N* O* b" a# Yshow that the leukemic clone remains detectable, as we have previously shown in
U4 l7 E7 y) k3 _! @( e4 \imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
/ y0 C+ v# r8 m8 q* d/ ^the emergence of clonal T cell populations, were observed both in one patient+ Z9 e: _' w; z1 C
who relapsed and in one patient in remission. Our results suggest that the
/ f% X5 a4 H9 E9 q; s, mcharacteristics of complete molecular response on dasatinib treatment may be# x" ?- t* I8 S. q! e, T
similar to that achieved with imatinib, at least in patients with adverse
0 {$ R- S" A4 ]1 T# wdisease features.
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