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。
' z0 Y. a! Z% o: _ 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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% n( `* G+ P1 d% @作者:来自澳大利亚% Z. m" _& f7 G
来源:Haematologica. 2011.8.9.
4 f1 G+ M! T( b$ pDear Group,
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: r! t2 F. c# L6 m3 ~Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML( D6 x% V5 ^+ K7 x t/ G
therapies. Here is a report from Australia on 3 patients who went off Sprycel
- |" O U, F6 W" c+ _4 O; [+ j% Hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients" V' W$ [- K6 }
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
7 [. R5 J- Y( p4 U. Q6 Edoes spike up the immune system so I hope more reports come out on this issue.6 P! T1 ?6 i) i5 X; s5 ]% Y3 l
J9 N% o8 C8 A7 mThe remarkable news about Sprycel cessation is that all 3 patients had failed
3 l- G! Q6 u0 ~- L+ s7 fGleevec and Sprycel was their second TKI so they had resistant disease. This is
1 x; f; F2 d I: n8 A* P5 Xdifferent from the stopping Gleevec trial in France which only targets patients2 n' O1 ]$ s$ u5 u# v$ S
who have done well on Gleevec.
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% L- K* \6 B/ L5 R+ u! b# x# DHopefully, the doctors will report on a larger study and long-term to see if the
2 [: m" [ R2 z1 L" M' b, Presponse off Sprycel is sustained.
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; q2 h h1 ^/ V, EBest Wishes,
: F7 H4 E) t C3 V0 W1 C$ G/ r; wAnjana3 ^. B0 z6 N& X0 q+ y# S
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Haematologica. 2011 Aug 9. [Epub ahead of print]
; ~" k5 W. N) b1 v6 ]5 d; LDurable complete molecular remission of chronic myeloid leukemia following
( R- j* L# Z5 [dasatinib cessation, despite adverse disease features.
8 F3 J, p: r1 }7 p% H6 bRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.# A# z6 [5 i& `
Source7 b# V* v1 _' X% h2 ?; x, I- b
Adelaide, Australia;
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Abstract
. m' h1 I3 }+ R& p! TPatients with chronic myeloid leukemia, treated with imatinib, who have a
/ H8 x3 S( k+ z m9 Rdurable complete molecular response might remain in CMR after stopping7 a) O. r& z' G3 T+ E
treatment. Previous reports of patients stopping treatment in complete molecular' X) i5 A; U2 z C
response have included only patients with a good response to imatinib. We
: Q$ k A$ P# ]. A r0 `0 jdescribe three patients with stable complete molecular response on dasatinib% D m9 O( M5 \
treatment following imatinib failure. Two of the three patients remain in
+ v$ v2 |6 P, q% I" ncomplete molecular response more than 12 months after stopping dasatinib. In9 ?, c! J4 C/ J# C6 G
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ W0 w+ p7 @/ _9 \' L
show that the leukemic clone remains detectable, as we have previously shown in$ Q* e( g& E% ^& W( M8 R
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
9 K' T! k3 _7 n6 M6 {. N* ~4 ]8 _$ dthe emergence of clonal T cell populations, were observed both in one patient- q4 B& Z, r; G+ f1 K* T# x; M% Y
who relapsed and in one patient in remission. Our results suggest that the
2 L7 |8 e% }& y" S+ L* U1 E1 ~characteristics of complete molecular response on dasatinib treatment may be/ I4 `% U/ U8 }; s" [- x
similar to that achieved with imatinib, at least in patients with adverse
4 {: _# T+ i% x9 E9 k% @6 Odisease features.
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