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。# L2 m0 y6 d8 w2 B6 e# I- C# B
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。
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作者:来自澳大利亚1 W* s, w; [' b
来源:Haematologica. 2011.8.9.
0 {' ]& C8 m0 a, n1 ~. \: gDear Group,! c3 P' a; f3 O6 y
8 Z' v9 R) ?; `: m ^Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
8 l. Q# L, n0 H) L& A3 K: H P1 Q! Stherapies. Here is a report from Australia on 3 patients who went off Sprycel
6 f. m7 K6 F4 h2 x& i9 Tafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
3 l8 U4 e0 U4 p$ w' `2 q7 qremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel n1 p6 F) K% ? f: E
does spike up the immune system so I hope more reports come out on this issue.4 s4 ~) ^- z# N6 n
8 t+ E r$ ^# ^( J$ e$ z6 ~The remarkable news about Sprycel cessation is that all 3 patients had failed8 i9 p* @4 A7 H P
Gleevec and Sprycel was their second TKI so they had resistant disease. This is! l) E: K+ @" k A' a+ `
different from the stopping Gleevec trial in France which only targets patients
7 n9 Z) }4 G& T( Cwho have done well on Gleevec.
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5 b: ]& T5 g$ U& D: Y- q. IHopefully, the doctors will report on a larger study and long-term to see if the
6 c' [6 h) v% G( w& presponse off Sprycel is sustained.
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Best Wishes,8 ~: @ q$ w1 P; E8 R9 G0 [
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]4 ~; O f# m i4 T" W3 j1 }
Durable complete molecular remission of chronic myeloid leukemia following
G% o) B9 Q0 ?( T& I. Edasatinib cessation, despite adverse disease features.
3 t% |& }. e- @% k1 L" VRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.4 O! n- a8 M, w" e# T7 u
Source
" Y/ X8 u4 {" h g8 QAdelaide, Australia;
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, U5 `* I9 _7 v) wAbstract
) \0 u; f6 z6 h# @& Y1 [Patients with chronic myeloid leukemia, treated with imatinib, who have a5 ^2 n) o8 S7 ~% }
durable complete molecular response might remain in CMR after stopping
. G( C4 L, l' d& {% A& d* x4 qtreatment. Previous reports of patients stopping treatment in complete molecular
, {8 g9 [; T$ {: presponse have included only patients with a good response to imatinib. We8 Z' r7 Z) k4 N
describe three patients with stable complete molecular response on dasatinib
. w9 j( x: x$ i) w' Y% ~8 |- r, jtreatment following imatinib failure. Two of the three patients remain in
0 R, Q' U) C- ^complete molecular response more than 12 months after stopping dasatinib. In
- \& R% p8 \( _3 {these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) j0 b5 H- h, T3 u$ h& K; c. \show that the leukemic clone remains detectable, as we have previously shown in
# U2 L1 v" N; R( d: Jimatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 E, w4 V( E8 U J! `
the emergence of clonal T cell populations, were observed both in one patient4 O$ p. P! n: w5 `$ |7 w
who relapsed and in one patient in remission. Our results suggest that the8 f0 _4 w$ e7 N
characteristics of complete molecular response on dasatinib treatment may be
- P! i; Z6 Q! ~9 a1 qsimilar to that achieved with imatinib, at least in patients with adverse0 c7 Y, e; k& W& _. S
disease features.& g! l* t3 i1 k* p1 w1 }/ a
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