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。: X- Y8 z' h& ~
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。* i9 m( w9 `7 I
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作者:来自澳大利亚: t/ M6 ~3 E7 D& s; W. x; u& s V6 |; P
来源:Haematologica. 2011.8.9.$ d0 E+ ~+ r+ E S O
Dear Group,. s+ g* e$ V1 S) d' l- j1 s
4 {4 \8 E; o5 oSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 i/ P0 M# s% X1 }+ |therapies. Here is a report from Australia on 3 patients who went off Sprycel
) {! H4 S M" x1 e8 q: C, rafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients" O0 e/ n2 s% }& r
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel" j' J+ G1 d+ \* V& G. N. e
does spike up the immune system so I hope more reports come out on this issue.
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, F/ @* _, |$ W+ MThe remarkable news about Sprycel cessation is that all 3 patients had failed: Y9 T+ {6 A$ O7 f( C
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
8 }+ j1 p. J% O# v `4 T2 D( {different from the stopping Gleevec trial in France which only targets patients- E5 l4 E( ^3 A. x) j f Q3 r$ P
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
9 a$ Z/ Y$ _5 c4 g: H' Mresponse off Sprycel is sustained.7 @( J) p- f4 S
0 s& V$ E, `3 |9 LBest Wishes,$ W, X+ Q. ^* r6 y/ I: M4 {6 o3 `
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]9 ?: ?4 K0 w, f, v& r& i' {
Durable complete molecular remission of chronic myeloid leukemia following" Q2 A+ V2 a* j+ }+ U, u8 l
dasatinib cessation, despite adverse disease features.
! @9 k, r+ u1 h! ]0 H' ZRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
& Z% t& |; X2 }1 ^; X6 LSource
$ w8 m. M |& M7 K4 L2 M" ?+ HAdelaide, Australia;. Z1 Q1 T/ N: q! h f& j
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Abstract& t, T, {: K! F5 ]
Patients with chronic myeloid leukemia, treated with imatinib, who have a8 V. I/ W. \# z- Z) P5 Z
durable complete molecular response might remain in CMR after stopping. j! x$ @, k9 i' v8 i$ `
treatment. Previous reports of patients stopping treatment in complete molecular
& U+ Z1 d7 n8 \. P9 d+ wresponse have included only patients with a good response to imatinib. We) ?* D7 R; b9 D8 w H
describe three patients with stable complete molecular response on dasatinib
: |; p0 {: d; T! _8 g9 [6 ]treatment following imatinib failure. Two of the three patients remain in
5 e' P$ ?7 G+ Y! G! f' @complete molecular response more than 12 months after stopping dasatinib. In1 k* K; }2 o7 C
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to' e0 M* \% e3 q" M& x
show that the leukemic clone remains detectable, as we have previously shown in' i1 U/ H6 P4 R* F' B/ @/ C6 E
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as* r, i# f! B$ t
the emergence of clonal T cell populations, were observed both in one patient4 t% F% T* U" k
who relapsed and in one patient in remission. Our results suggest that the0 ?/ s: D0 T! B @
characteristics of complete molecular response on dasatinib treatment may be
* L/ A- @2 e, y+ V1 w9 |. w/ Rsimilar to that achieved with imatinib, at least in patients with adverse" G3 c! w: v# L1 W$ C" x* s1 S. A
disease features.
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