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。% N, |: g! K* v0 z
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。( N( l" X6 p. i% p- H+ p
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作者:来自澳大利亚
+ o3 E. v: X" p0 y/ h5 D4 H( t来源:Haematologica. 2011.8.9.) E+ ?; ^; X3 T0 L3 f
Dear Group,! p- f! T" H% u2 F: e% X3 y
# z5 h3 c4 T/ A- f; f( o+ A: B3 _Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 ~! \% Z- Z, rtherapies. Here is a report from Australia on 3 patients who went off Sprycel
, @; y, B( ?# h: F, n& iafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients. P) K! v- T( I9 X
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
+ O& T, Z5 E) R; l2 E1 fdoes spike up the immune system so I hope more reports come out on this issue.) @5 W: a. d% ^( }% g, [6 L. N
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The remarkable news about Sprycel cessation is that all 3 patients had failed
/ _% R2 U, K4 a* CGleevec and Sprycel was their second TKI so they had resistant disease. This is
9 d7 v6 V& |2 T2 a' N2 h) }" W6 Q0 ^different from the stopping Gleevec trial in France which only targets patients
: p- @# |8 [9 C9 x: i# Y! U1 ?who have done well on Gleevec.! a% e- ^. E- |7 X6 @6 t' K
8 F1 d7 R3 x% E' y; d2 [. bHopefully, the doctors will report on a larger study and long-term to see if the
- ?6 K4 @; [2 lresponse off Sprycel is sustained.
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1 M! F; a- }, Q dBest Wishes,
6 A# b! ^9 v* ^& S- R# nAnjana& w* h5 x3 r. U* N
4 E* N* Q4 E/ d7 P9 z/ w
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6 M- [3 |2 q6 G3 M) i' a; ?Haematologica. 2011 Aug 9. [Epub ahead of print]+ e% Z: a) ~6 y
Durable complete molecular remission of chronic myeloid leukemia following
+ U. {+ d/ S/ E3 D; v" M3 l9 C( f7 vdasatinib cessation, despite adverse disease features.; e7 T2 U1 |; C1 N2 C6 E
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.9 Z, L7 d6 r4 ]. C4 B: F
Source
8 ~; ]0 \* R$ R$ mAdelaide, Australia;
6 G" a9 X0 m+ \, A- h6 F0 m3 s- y6 T- V7 s6 X8 R
Abstract8 M: L1 k; a2 h3 z" d& b
Patients with chronic myeloid leukemia, treated with imatinib, who have a
$ X% Y* [% V0 o& r# D2 c/ Gdurable complete molecular response might remain in CMR after stopping
9 m+ }( \* s) ]% a5 j: Atreatment. Previous reports of patients stopping treatment in complete molecular
' W3 r; k4 ]9 K- _6 J! Z) b/ Nresponse have included only patients with a good response to imatinib. We# Y/ q- X& g% N3 p: i0 [1 x
describe three patients with stable complete molecular response on dasatinib4 m: u/ t3 ]$ t1 T) J9 q
treatment following imatinib failure. Two of the three patients remain in. V' G& M/ K, u4 i7 D
complete molecular response more than 12 months after stopping dasatinib. In& a4 ^% U. ?/ F% S; D7 a9 i
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to5 F- g' Z, \; [
show that the leukemic clone remains detectable, as we have previously shown in
: ^+ q a' D+ b7 dimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
0 y( y8 _3 P$ }6 ]' L8 ~3 _2 Vthe emergence of clonal T cell populations, were observed both in one patient
# |6 b( Q- ~1 A! f8 |5 I* [! cwho relapsed and in one patient in remission. Our results suggest that the6 f3 Z+ r- g+ q/ k
characteristics of complete molecular response on dasatinib treatment may be
^8 p# A- r$ g' dsimilar to that achieved with imatinib, at least in patients with adverse# l c, d3 S q$ Y9 S" U
disease features.
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