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。
; Q3 Y, i7 U: K$ v5 Y; Y 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。) O9 e6 |1 z; E9 B$ i, v) p
5 h0 `# Q. {$ E% F( O! R作者:来自澳大利亚1 s; E7 \- F5 w% @
来源:Haematologica. 2011.8.9./ u7 C" A" I; k8 [; t! h
Dear Group,/ I9 ~! R; {, B* S' q- t( d9 ~. G
' h( G- _6 _! V) i2 j, n) PSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML) ?; `+ y. S7 R5 T k1 Y& S
therapies. Here is a report from Australia on 3 patients who went off Sprycel$ G0 `7 w. E" l( ^
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
. Z. ?; `, K* _8 @+ j! P+ T6 E3 Premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
+ \1 P9 l7 A K& z3 w7 d0 xdoes spike up the immune system so I hope more reports come out on this issue.
' o3 d K1 o( g$ h7 P5 H. Y/ [ Q; |. R
The remarkable news about Sprycel cessation is that all 3 patients had failed
! A5 X9 ?( i% }, `Gleevec and Sprycel was their second TKI so they had resistant disease. This is
& k! K& U0 g5 vdifferent from the stopping Gleevec trial in France which only targets patients5 }* T! y( [3 v8 V C L5 I7 E, _! J2 b
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, [ ]! B: i/ d" r( m6 |- x3 j
response off Sprycel is sustained.) i: R- L0 `1 t r; q, X) j
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Best Wishes,
+ c u5 R% c/ w# D- dAnjana/ l" T2 Q) }2 c% ]
% e0 i9 ~' k9 N' r% }
3 K- R+ w8 H# f1 ^2 V1 V
# g6 U* j6 S$ X+ I, s4 MHaematologica. 2011 Aug 9. [Epub ahead of print]
7 W% _& B) q) K" M& Z8 d8 p& r" UDurable complete molecular remission of chronic myeloid leukemia following
; |- S1 M, D: R4 b* [9 ?dasatinib cessation, despite adverse disease features.
7 Y P' W# z9 |( V- a! I. v( \/ QRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
7 F" [; m+ P6 c/ }8 u- w, S$ WSource. h2 j% I; t6 ?) |
Adelaide, Australia;
7 o! n3 t. r9 T: V1 a! V3 o- S) x1 X
- Z' B+ d+ G8 w0 A% u6 ]Abstract
7 g {! ^+ z+ Z8 ?Patients with chronic myeloid leukemia, treated with imatinib, who have a
* ~6 `5 {8 m* k% | n! P% O5 `' sdurable complete molecular response might remain in CMR after stopping
% a4 e/ }) q& F1 Y8 Itreatment. Previous reports of patients stopping treatment in complete molecular3 n* z M6 t5 N
response have included only patients with a good response to imatinib. We( g# p) _9 U$ ]
describe three patients with stable complete molecular response on dasatinib
7 Z: O+ X% D% @; @' Etreatment following imatinib failure. Two of the three patients remain in
" ?8 b8 S' f; o. J; y- Xcomplete molecular response more than 12 months after stopping dasatinib. In4 R3 }8 D8 y! v J% |# F- e
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to2 L/ ]8 j3 x# R. |
show that the leukemic clone remains detectable, as we have previously shown in+ o7 E2 a( ]2 Z
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as3 _ \+ d4 w; |) i7 i$ `
the emergence of clonal T cell populations, were observed both in one patient
" U9 Q2 w4 i6 j3 Pwho relapsed and in one patient in remission. Our results suggest that the
x+ I5 e5 D/ T& e6 O- r4 Ucharacteristics of complete molecular response on dasatinib treatment may be5 S8 g( h. S7 `$ t" F5 i
similar to that achieved with imatinib, at least in patients with adverse0 b# T- \$ H3 C
disease features.
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