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。
: W' f) J ], D7 Y6 k" ~; 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。9 k& |( l% ~3 a' @
: j$ Z+ C0 V, S M作者:来自澳大利亚- S$ ?% n+ k! D' s. ?: F) ]( |6 z! S
来源:Haematologica. 2011.8.9.
: e8 ^9 n( ?7 Q7 Y8 T' _" dDear Group,
9 {+ v4 Q$ S1 ~, ?- Y2 n! P, T. J8 h. \. C2 [8 w
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
2 W* C! t( g) ~( g$ Ftherapies. Here is a report from Australia on 3 patients who went off Sprycel
9 Y' A' o$ }9 Y9 K" @after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients) c" l7 M- Y3 ^. m% M- V
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# j2 P& z3 i6 |5 B) ydoes spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed
, h7 d5 g2 y( kGleevec and Sprycel was their second TKI so they had resistant disease. This is
& G! _2 h$ K% Idifferent from the stopping Gleevec trial in France which only targets patients9 U% t. \0 W8 B
who have done well on Gleevec. u. q/ T# u. ~& k0 Y) K
0 e& T- r1 M3 k+ c3 r0 bHopefully, the doctors will report on a larger study and long-term to see if the
, Q. S7 G/ B* m% V+ Rresponse off Sprycel is sustained.
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Best Wishes,3 x* G7 {8 H- R6 @4 a
Anjana
9 k1 {+ I6 G9 ?3 J; ?: u [1 K( M: p1 c
, y7 w! @9 G9 S* S) ~" c& }, _- i. O3 c# J
Haematologica. 2011 Aug 9. [Epub ahead of print]
# {' l7 H) A; Q; X( V7 JDurable complete molecular remission of chronic myeloid leukemia following& i: Q( i. \1 ?3 L! i5 V
dasatinib cessation, despite adverse disease features.
1 x' L/ ^; O! w* c* i, TRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
/ E/ Q! M" n2 W% T: [0 Q/ {3 PSource
. l& d4 y7 K& H ~Adelaide, Australia;, F3 P) l1 ~" [
& z6 ] f7 j7 g4 T9 `- UAbstract! e7 U4 [# w: {) ^0 M) c3 [
Patients with chronic myeloid leukemia, treated with imatinib, who have a2 w5 |. A/ Y" Y, q4 c& K/ P7 e
durable complete molecular response might remain in CMR after stopping
* Y4 M. O( ?$ v: utreatment. Previous reports of patients stopping treatment in complete molecular
6 t; i8 n8 x+ N, R8 Dresponse have included only patients with a good response to imatinib. We
9 W: @) p p. E t$ t4 \# ddescribe three patients with stable complete molecular response on dasatinib
. R& @7 j- a& a2 l) V$ x, vtreatment following imatinib failure. Two of the three patients remain in+ X! N% v& F' h: h q. h) Z3 I1 x
complete molecular response more than 12 months after stopping dasatinib. In# w0 e/ ~& e ~
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
- [8 k; l4 e! g2 cshow that the leukemic clone remains detectable, as we have previously shown in k7 j- y! I8 [' y! s1 i7 [% R
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as) V7 z0 P r } _; }* ] f! g
the emergence of clonal T cell populations, were observed both in one patient
1 x7 p8 l0 F8 \- M& xwho relapsed and in one patient in remission. Our results suggest that the
, p% f& v: r* M# b0 O7 z6 [$ ncharacteristics of complete molecular response on dasatinib treatment may be
# V |8 \. c$ d- t/ ysimilar to that achieved with imatinib, at least in patients with adverse _( _' ?0 V) ~, w
disease features.
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