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。/ c6 o- r. u( D: c( C- \2 U
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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9 J4 j! Q: \ P3 k) f& k( w1 `! p: J作者:来自澳大利亚+ N# ?! d$ n- v7 Z
来源:Haematologica. 2011.8.9.
2 a4 \$ I1 K/ XDear Group,* J/ g! E# [8 {: i- l
2 {$ }/ K6 u2 V6 n! S: FSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
x0 y$ x# Z( `" r% _therapies. Here is a report from Australia on 3 patients who went off Sprycel
7 E( T$ h( f' J4 K! Mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients& ?" D c$ ~ E# [# I2 w
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
2 ?/ B) B, M) M7 U' f! B3 Gdoes spike up the immune system so I hope more reports come out on this issue.* [$ Y% x. S7 m- u
. A( ?' T# _, @& e* c; {% q& g' XThe remarkable news about Sprycel cessation is that all 3 patients had failed% P0 [' g( e* S+ N, u
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
0 z0 Y0 x/ M' J+ u9 B( {different from the stopping Gleevec trial in France which only targets patients& V( h, H- L: Q% q
who have done well on Gleevec.
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7 v$ i1 ]' g7 {Hopefully, the doctors will report on a larger study and long-term to see if the
$ S" _& D9 J+ N2 {response off Sprycel is sustained.+ e' E# o1 C) V$ K7 ~$ x
, A) M) m% @. h1 [9 Y
Best Wishes,
) K6 g, Q0 \% @/ d( h( K1 ?; FAnjana) C4 Q: y4 n0 S% ?$ j/ x! T+ ]: ~
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; I+ J3 P8 g4 w) @! x' ?7 RHaematologica. 2011 Aug 9. [Epub ahead of print]
, M# T. c5 V. N4 v4 \Durable complete molecular remission of chronic myeloid leukemia following
, y [6 T$ v: `) @( _# hdasatinib cessation, despite adverse disease features.
6 i. I' ^ b+ u( D- }& e$ G9 t, |Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.) b4 ~2 {# y" r9 ` N
Source* N O5 A. o. N" p1 w6 a3 I2 o
Adelaide, Australia;( l* F% N! W* ]1 W
: p( \/ Z$ Q0 F; w3 jAbstract
' F7 c7 n; D- r$ ]: Y; SPatients with chronic myeloid leukemia, treated with imatinib, who have a
5 l0 Z8 u( V4 L; Odurable complete molecular response might remain in CMR after stopping
0 x% T* |' H* N! x/ v; G5 Jtreatment. Previous reports of patients stopping treatment in complete molecular" E2 T _( l! A, }. ?
response have included only patients with a good response to imatinib. We
* G) [, m; Q3 {" T; M% n% m) [describe three patients with stable complete molecular response on dasatinib
_; e" n/ d2 A% m% @, d8 n0 Htreatment following imatinib failure. Two of the three patients remain in
/ \4 [9 k; \3 Y8 ]complete molecular response more than 12 months after stopping dasatinib. In7 I1 x6 _2 @* P3 j4 i
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' J S0 e# P s8 w( y5 L5 `show that the leukemic clone remains detectable, as we have previously shown in+ a# a! \7 E; u1 a K! v4 Q
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- i- k7 u1 z1 y1 v- b
the emergence of clonal T cell populations, were observed both in one patient* s4 V7 f+ ?2 g
who relapsed and in one patient in remission. Our results suggest that the
^' }" A0 W1 h- M; x+ d1 B8 ]' bcharacteristics of complete molecular response on dasatinib treatment may be
8 B) \ k& W$ xsimilar to that achieved with imatinib, at least in patients with adverse1 q; B$ o7 T7 f
disease features.2 E' M$ ?$ h S* ^
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