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 `, G! {2 v: O7 p 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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D7 P. y8 a! u作者:来自澳大利亚) m/ b! _. m( L
来源:Haematologica. 2011.8.9.
$ s! {, g2 `4 M, c) s% S: J9 M9 }Dear Group,
1 ?2 B [" Z& ]8 p1 R
* ^6 ~* s- C! f# s8 dSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: T: j9 a2 y+ f, E( f! {! S1 wtherapies. Here is a report from Australia on 3 patients who went off Sprycel
; p( g& \% ^2 r, W4 \2 kafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients9 A8 T8 w- [$ U& u ^
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel3 p8 Q6 ~% I* r: `" e. E: w
does spike up the immune system so I hope more reports come out on this issue.7 G8 \' u3 w7 B+ T, y g `. P
* l8 U$ l5 l4 G j5 G' _2 ?The remarkable news about Sprycel cessation is that all 3 patients had failed
X( f9 R8 @4 u6 S9 GGleevec and Sprycel was their second TKI so they had resistant disease. This is
& ~- t/ ^5 H- a( l8 `* S! X6 ~different from the stopping Gleevec trial in France which only targets patients, S! G6 Y; Q. F8 z2 p1 C
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 the9 e7 d; K2 c2 X3 m& A
response off Sprycel is sustained." d, ^6 o# v8 a' Y `
9 A9 X3 B" m9 D" M9 ~6 WBest Wishes,
- D2 t1 j( O- y) C6 b5 aAnjana g* K, q8 T% l9 \
2 W! P f6 E& X& i: I. h9 Y+ V' E( O+ g2 T5 S
& k8 c7 P/ \* U" yHaematologica. 2011 Aug 9. [Epub ahead of print]
+ B. G1 f4 i& NDurable complete molecular remission of chronic myeloid leukemia following3 `; Z' @2 Q8 C0 n0 Z$ c
dasatinib cessation, despite adverse disease features.
. @3 \7 V5 j$ ^4 v: f8 O% k0 LRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( @4 t1 c! o% r' N
Source' Y8 S6 }5 N* B7 f+ V" E% c
Adelaide, Australia;/ A7 b& v( w8 N3 e
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Abstract" L& s7 L' ?3 Y n) m: P
Patients with chronic myeloid leukemia, treated with imatinib, who have a
; R$ E2 b; _& m7 ddurable complete molecular response might remain in CMR after stopping! P( Z: G. w9 w' b; x6 O
treatment. Previous reports of patients stopping treatment in complete molecular5 n3 d( k) K0 g0 _8 G5 D6 V
response have included only patients with a good response to imatinib. We0 A5 b' a* M) I$ F c$ c' ]% Z
describe three patients with stable complete molecular response on dasatinib
, k: A7 e4 ]. c/ u, _; }treatment following imatinib failure. Two of the three patients remain in
- K7 b* W8 n5 ?. G# Qcomplete molecular response more than 12 months after stopping dasatinib. In; i U5 g4 R- u! f# B" v# y' d% M5 B: K
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
, L7 o9 N0 z- C6 a8 W; Dshow that the leukemic clone remains detectable, as we have previously shown in# t4 N: o0 j% j# o
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
; Z" E! u6 I& f1 f" S# b, y& Sthe emergence of clonal T cell populations, were observed both in one patient9 x4 ~% V1 U( `0 ]3 _5 l
who relapsed and in one patient in remission. Our results suggest that the
& y1 J; J X6 j9 p' u) rcharacteristics of complete molecular response on dasatinib treatment may be
_# K5 |1 H/ k/ C- I' {similar to that achieved with imatinib, at least in patients with adverse8 z; t7 ~5 k( l8 j+ |
disease features.
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