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。
c0 Q; z3 I4 }5 J$ g/ r 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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9 E- Y: D0 X% r$ Y$ N2 |9 U作者:来自澳大利亚: r6 v* x% ` a2 ~
来源:Haematologica. 2011.8.9.( ~" K& e& ^# ~+ D1 n/ m
Dear Group,; M+ N& Z9 p/ X% X
# O' [$ |" ?0 O% I6 VSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, }" o" e1 r% Y8 Q9 A& {) y, o" m5 ftherapies. Here is a report from Australia on 3 patients who went off Sprycel
3 C: i8 W# n) R/ v' i& _6 B; ?after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
! J. M* [) @, U4 ^: e* P6 b& z& c; _% eremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
e- I2 j9 h9 ~+ x; @6 _) rdoes spike up the immune system so I hope more reports come out on this issue.7 j8 h$ e9 \6 O0 j9 y9 p
, r$ R: W4 g6 y5 r4 vThe remarkable news about Sprycel cessation is that all 3 patients had failed
- [2 y }4 x# _ p5 i* b) V: mGleevec and Sprycel was their second TKI so they had resistant disease. This is3 Y" H" s$ S! e
different from the stopping Gleevec trial in France which only targets patients
|; ?' _3 k* J" uwho have done well on Gleevec.+ t4 l$ V0 l$ y. o' |2 L
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Hopefully, the doctors will report on a larger study and long-term to see if the
3 c- |! f& J+ Yresponse off Sprycel is sustained.
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Best Wishes,
) _2 G. W. L9 J G! Y+ }Anjana! }4 _7 e% @* l: ?0 ]& w* {
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7 ^% P6 N( T. ~ P( @* p( ~ uHaematologica. 2011 Aug 9. [Epub ahead of print]9 ^; b% j4 V$ Q; @ p' d) q5 a
Durable complete molecular remission of chronic myeloid leukemia following8 O7 }* d4 i! O3 |5 u
dasatinib cessation, despite adverse disease features.
) x4 U. F* K, V* pRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP./ [5 }( F* P. V2 q# V
Source8 v7 i& j6 G N
Adelaide, Australia;
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Abstract
9 N0 ^; s/ {5 V9 ~! sPatients with chronic myeloid leukemia, treated with imatinib, who have a
% o" T( P0 Z4 {! Y Ldurable complete molecular response might remain in CMR after stopping0 N; A- Q$ U' d+ ], p% |
treatment. Previous reports of patients stopping treatment in complete molecular d6 Y; g5 x$ ~/ @2 t3 K$ V9 Z
response have included only patients with a good response to imatinib. We: O9 d, b4 V% O: Q0 w7 W* ~" |' Q
describe three patients with stable complete molecular response on dasatinib
- F4 Q0 g, Q1 _4 ]& ^treatment following imatinib failure. Two of the three patients remain in: ^9 k4 N# C% f5 N5 _5 J/ k
complete molecular response more than 12 months after stopping dasatinib. In6 Q# \' w* y$ u' a# e
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to* q1 h6 `2 C/ e. }8 }2 ] B
show that the leukemic clone remains detectable, as we have previously shown in. @% e0 `, C4 |4 x3 j
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
1 b8 |$ ^3 L; f! X, Mthe emergence of clonal T cell populations, were observed both in one patient
8 T( k6 h& T% W, n/ l0 nwho relapsed and in one patient in remission. Our results suggest that the5 y8 g. r6 l( a: D/ d3 {+ z+ ]
characteristics of complete molecular response on dasatinib treatment may be# q/ ?4 P& @3 C) c6 ^, ?
similar to that achieved with imatinib, at least in patients with adverse
7 _& D! U: M, _- d) |disease features.
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