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。" ?3 x9 ]8 J) h, a, d4 e
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
8 p' L# {9 j3 k5 w来源：Haematologica. 2011.8.9.
; j1 \+ K: X( q- F! pDear Group,+ x# S% ]7 q* _: u& z( O0 f
+ c( j( Q8 O, {: S2 g' Z) I4 v
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML. w% q7 y' i5 E' ^ G' v
therapies. Here is a report from Australia on 3 patients who went off Sprycel
8 E' g; b6 m" G" j% I1 I1 h" c$ Lafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients( c3 c- _# f7 Z) [( N: `
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& H7 c9 u( r, Q2 u {, ndoes spike up the immune system so I hope more reports come out on this issue.. N7 L* h2 ?2 D/ A% \: E% x4 v" v
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The remarkable news about Sprycel cessation is that all 3 patients had failed: U* @- x) }0 g
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
* V2 {/ c' |1 o/ \& y6 A( ^different from the stopping Gleevec trial in France which only targets patients% o* F% b; h% l
who have done well on Gleevec.
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2 I, M9 j" P& OHopefully, the doctors will report on a larger study and long-term to see if the
3 I3 B& E6 g" v; q& B) tresponse off Sprycel is sustained.
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1 I% ?& P$ ~0 s0 ~9 |* k9 S8 O- S( hBest Wishes,
' o) H. {* ~# q! o6 b7 R9 jAnjana" I4 w9 ^: e! r' `2 o( f7 p
z2 M# j; x3 y/ S8 \2 P
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Haematologica. 2011 Aug 9. [Epub ahead of print]: I2 u4 t* P+ d; a
Durable complete molecular remission of chronic myeloid leukemia following
4 Q% q5 `7 H. R; udasatinib cessation, despite adverse disease features.; P, n* @2 Q' P* }3 M* K
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.2 W+ U' S; v) w- N( s( `( v% ?
Source
+ `% J% Z9 N' i2 C5 t% B+ C# sAdelaide, Australia;! i: `) @$ Y7 [8 I' Q a
: B# P/ F2 x3 Y6 N( I% E2 s7 B- CAbstract5 N* {1 d+ y& \, Z$ v7 k. m% R
Patients with chronic myeloid leukemia, treated with imatinib, who have a/ e: R& u5 Y- G& q. \- R8 A
durable complete molecular response might remain in CMR after stopping
: k/ Q3 w& Z& A, x* R2 Qtreatment. Previous reports of patients stopping treatment in complete molecular
( I' u+ I8 v3 R: @6 a4 jresponse have included only patients with a good response to imatinib. We* ?1 A! U. R% I
describe three patients with stable complete molecular response on dasatinib
6 d. i3 d" X N H% \4 K+ ktreatment following imatinib failure. Two of the three patients remain in
E) P& z6 e; O# @complete molecular response more than 12 months after stopping dasatinib. In
! y/ t7 A, a. F2 y/ Q [these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
; h3 m M& A0 c z6 n. ^show that the leukemic clone remains detectable, as we have previously shown in
) ]" x3 B% ]% h7 ^imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
0 [7 s, e. s: h0 J4 y2 J% p. a+ Tthe emergence of clonal T cell populations, were observed both in one patient! v0 ^5 n% c* ^. k' e
who relapsed and in one patient in remission. Our results suggest that the% }+ ?+ g& x: b% i+ A
characteristics of complete molecular response on dasatinib treatment may be# R) |4 c7 k. e. H
similar to that achieved with imatinib, at least in patients with adverse
0 m5 Y2 b u% a2 _( Wdisease features.: s- F1 a9 a* C
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