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。 t6 F* W. k6 V3 c- n* v
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。$ {' t# `4 x u/ C+ k7 U) Z
7 N g2 J# _, p作者:来自澳大利亚
, l. Q. B% m7 {$ }来源:Haematologica. 2011.8.9.' Y G6 k- f1 R7 c
Dear Group,
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9 |3 D0 \6 v- K: GSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
6 _- _- Z1 }* O1 d, Jtherapies. Here is a report from Australia on 3 patients who went off Sprycel* [5 W( L) U; \; t+ y
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
4 p; d O' r, i; sremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 L( m$ ~3 N- c4 p8 J8 ^; W2 L0 J
does spike up the immune system so I hope more reports come out on this issue.4 M Y) p: e7 Z
, b7 P# r% E" N& s, AThe remarkable news about Sprycel cessation is that all 3 patients had failed9 S$ Y5 E Q( P1 l
Gleevec and Sprycel was their second TKI so they had resistant disease. This is" o) W& G( Z7 Q
different from the stopping Gleevec trial in France which only targets patients
+ x# f5 H! c4 Y# C" p: z8 q4 x) N* Gwho have done well on Gleevec.* ], h9 E0 s$ l: p5 u8 e0 r; n
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Hopefully, the doctors will report on a larger study and long-term to see if the
+ D/ R0 F3 M. e: P7 W2 q1 dresponse off Sprycel is sustained.. Q9 ~, u5 k2 z
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Best Wishes,6 F, |. [' i& K" w
Anjana6 ]; M4 ? M( {8 y" a, C$ k( V
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Haematologica. 2011 Aug 9. [Epub ahead of print]5 W h8 m. i9 Q0 {8 }
Durable complete molecular remission of chronic myeloid leukemia following6 R: r5 }$ d+ p$ E, E
dasatinib cessation, despite adverse disease features.
1 s" `8 ?8 Q3 Z& i: ?# h& GRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP., }" o8 w( f) ?% I+ P" Z7 J/ H
Source
9 B9 Z7 X( \$ u$ d. g ^- GAdelaide, Australia;* j( u8 @: ~% r, P; G& o. [
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Abstract
. K* D# u0 B, }8 X9 DPatients with chronic myeloid leukemia, treated with imatinib, who have a4 S; y0 J( h, }! `
durable complete molecular response might remain in CMR after stopping
2 ^8 H- l' i4 v: B# n% O1 v% Gtreatment. Previous reports of patients stopping treatment in complete molecular7 p+ F* f& \3 x. d' W& V1 ?
response have included only patients with a good response to imatinib. We
2 [7 n. x" x* R: Ndescribe three patients with stable complete molecular response on dasatinib
* j, B+ P0 @* ]2 _/ |& ttreatment following imatinib failure. Two of the three patients remain in; g$ H4 t9 t0 T! J
complete molecular response more than 12 months after stopping dasatinib. In
: y3 I! o: h# ~1 l* b A' d e0 fthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
7 n$ d3 F" x/ b3 ?8 ~show that the leukemic clone remains detectable, as we have previously shown in
3 J5 d- ]1 [% u1 U% K$ F/ W8 |& cimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 w. {! _+ z/ Y' `! M% k2 bthe emergence of clonal T cell populations, were observed both in one patient
3 e, C7 {5 N" C' Z q0 I2 E) uwho relapsed and in one patient in remission. Our results suggest that the a6 K2 {: V- z2 u7 w* x
characteristics of complete molecular response on dasatinib treatment may be& I& V, v2 D+ Q: w& D2 D1 X4 i
similar to that achieved with imatinib, at least in patients with adverse' }* h4 G7 j1 M- L! e! |* Y
disease features.
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