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。
) ] g3 D5 q5 G# ` 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。8 l# L: j$ X+ Q2 f& j, W4 q
, A' Q N* g7 i' P: x作者:来自澳大利亚9 e8 A6 H# }5 R6 k' a* \
来源:Haematologica. 2011.8.9.
, i T& [9 a" @Dear Group,+ x1 B |- k, q; j
3 ^& P1 I: Z( ]# }
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
" f: T& O- m& j1 C6 q- Ctherapies. Here is a report from Australia on 3 patients who went off Sprycel
5 f. d9 o3 Q& Wafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients- c# y7 ^0 J" U' J7 P' J
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# N2 Y+ C+ h- n" u4 `" A1 W3 k' Rdoes spike up the immune system so I hope more reports come out on this issue.
6 x7 w' r1 _" J/ `
7 z# I! x( u$ G1 F1 gThe remarkable news about Sprycel cessation is that all 3 patients had failed% I4 U, I! j! y; V1 ?
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
$ n# r7 i# F( f5 ]. u: Y# \different from the stopping Gleevec trial in France which only targets patients$ r' S* _. o% Y& m- H
who have done well on Gleevec.. Z. X" n' k$ B. E7 D3 I) Q
3 Z. ?% `3 N J u
Hopefully, the doctors will report on a larger study and long-term to see if the
/ v/ ^7 e5 e& |response off Sprycel is sustained.
& F9 G" F1 l6 E& n( d7 V5 P+ p+ s4 Q$ z' x/ | Y
Best Wishes,/ D& ?4 b* Y+ Z4 H" }6 n( _
Anjana! ~- l/ z! F& Z# U- A3 m
% ^: x4 Y. B4 Y# b$ T
3 k" x8 {/ J: R# [3 X: F
2 E8 l0 r, Z4 w8 h4 ]# KHaematologica. 2011 Aug 9. [Epub ahead of print]3 A2 o- G) G' a( f0 E
Durable complete molecular remission of chronic myeloid leukemia following4 Y$ b/ t- T" e2 _5 d$ Q7 a
dasatinib cessation, despite adverse disease features.
/ v' u$ @" F3 YRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
, k" i/ b# y9 u0 N) t5 B: `( NSource% q" H$ ^9 z3 c" c
Adelaide, Australia;+ O( G2 ]) N- }; _
: P) b! [% `& q
Abstract
8 N1 D% O9 {6 M0 K- j5 S- d. aPatients with chronic myeloid leukemia, treated with imatinib, who have a" V' E! j1 s3 }, ~. V6 J
durable complete molecular response might remain in CMR after stopping0 } t% D5 w# w1 m3 h
treatment. Previous reports of patients stopping treatment in complete molecular6 {# x8 X4 u1 Z; h$ {, [' T
response have included only patients with a good response to imatinib. We
2 O1 q( K# |- l- {4 Jdescribe three patients with stable complete molecular response on dasatinib
4 N8 }& y3 S2 }0 f! G4 X r( U2 A1 b8 ^treatment following imatinib failure. Two of the three patients remain in. I$ r* l" d$ C9 n# d5 L
complete molecular response more than 12 months after stopping dasatinib. In
& _- D2 L7 j7 x& Hthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
$ R) k, E1 f7 T4 O3 s9 Z* ^* h( }, kshow that the leukemic clone remains detectable, as we have previously shown in
" V; u( B4 }; |7 J" Uimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
, P" y. U# b7 n2 athe emergence of clonal T cell populations, were observed both in one patient! f: ^0 P/ Z |* m
who relapsed and in one patient in remission. Our results suggest that the# v( T# i3 X9 }. H! ?
characteristics of complete molecular response on dasatinib treatment may be
$ G/ ^# u0 F) s9 A9 p8 psimilar to that achieved with imatinib, at least in patients with adverse& X3 h6 k. X7 r% s4 j1 U# V2 M" F
disease features.
- c* X% f; a P& ~/ d |