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。) R# ]4 n0 \9 F% F/ v# C5 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。4 x8 \7 h2 }! c/ {5 u1 K# O$ ~
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作者:来自澳大利亚% i0 M* i; R& s9 H* {% f; R
来源:Haematologica. 2011.8.9.% q3 j. n$ l2 q
Dear Group,' P3 [. q7 [1 I; l2 O6 s: h9 u
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
! T" d* `3 l6 X2 atherapies. Here is a report from Australia on 3 patients who went off Sprycel: o6 Z8 v% A% b- R
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
% X/ H4 `/ m& N6 `remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel x& s: V" n+ X d
does spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed0 [9 t4 y( n, L" A- h0 J
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
% X, S# g- N' {5 [different from the stopping Gleevec trial in France which only targets patients: V$ c2 b) `6 n
who have done well on Gleevec.
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8 u/ `6 S. n ~# L$ B$ _* qHopefully, the doctors will report on a larger study and long-term to see if the
& B3 k. Z$ {" S8 p" Eresponse off Sprycel is sustained.
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Best Wishes,
! l; J) z0 M$ zAnjana
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. y+ p2 i" u5 MHaematologica. 2011 Aug 9. [Epub ahead of print]
: U# u5 q' u2 n5 e5 n: ODurable complete molecular remission of chronic myeloid leukemia following
5 \ @* I, T2 {9 Jdasatinib cessation, despite adverse disease features.
* n5 V" A8 T- A2 e, u' g4 z4 oRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
9 X. h+ t7 k* l1 o1 z9 O7 s: GSource
( z- v0 P+ } T' s! }# K d0 U. ]" rAdelaide, Australia;1 y! R1 F; [* M; @) O3 T* D
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Abstract6 \% Q" O; b. z7 ]9 B0 q
Patients with chronic myeloid leukemia, treated with imatinib, who have a
; X, k* O+ Z. y1 k5 E3 T* p7 d! B( j% |durable complete molecular response might remain in CMR after stopping
( ?2 y( F. d( Z1 a) ~treatment. Previous reports of patients stopping treatment in complete molecular) E7 S `7 i% k" b( S, M4 s* H
response have included only patients with a good response to imatinib. We
3 E/ _. F8 |' U V, P8 E2 C+ Jdescribe three patients with stable complete molecular response on dasatinib
; t: u2 t0 |4 ~0 |0 Etreatment following imatinib failure. Two of the three patients remain in2 E F$ R2 l6 g4 J
complete molecular response more than 12 months after stopping dasatinib. In
- b5 @2 F) G) Z. l( [( O$ p. athese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) O. J+ P, m% Ushow that the leukemic clone remains detectable, as we have previously shown in
2 ]! t4 [( T0 h% z' A' D3 j6 mimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ S7 i, E5 Q4 h# Sthe emergence of clonal T cell populations, were observed both in one patient
' l0 `8 h( w& {% Wwho relapsed and in one patient in remission. Our results suggest that the
( C6 @* B7 T( I+ ^% vcharacteristics of complete molecular response on dasatinib treatment may be3 |+ u/ H) Z/ G$ z, y
similar to that achieved with imatinib, at least in patients with adverse
9 j$ E& i9 Z7 M ?6 d; r) Ndisease features.
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