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。
" {7 ?& I& q; r$ X% f2 T: }3 U 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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8 H+ I$ E7 }1 F6 V! d0 D9 \作者:来自澳大利亚' _: h& L1 e; ?/ q3 d
来源:Haematologica. 2011.8.9.. s p7 c H4 F K b) z
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" R* O2 K, @+ h& X( j; Y( Z, N
therapies. Here is a report from Australia on 3 patients who went off Sprycel
2 |: S! X7 q0 X& S7 e$ q* o0 {# W6 Gafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients# V6 S$ D! ?+ b1 j* F
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel: q- M- n5 t! a$ L2 H
does spike up the immune system so I hope more reports come out on this issue.
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H& W4 G% P7 s- IThe remarkable news about Sprycel cessation is that all 3 patients had failed
9 j0 I7 T- k2 }1 @& X7 U+ @6 D& BGleevec and Sprycel was their second TKI so they had resistant disease. This is8 ]; p" D/ k& n e
different from the stopping Gleevec trial in France which only targets patients; R5 \- P. @/ g; V8 m
who have done well on Gleevec.
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. {( G/ r& w6 F+ l1 _2 [! PHopefully, the doctors will report on a larger study and long-term to see if the
7 q4 m3 l( L( T+ l4 bresponse off Sprycel is sustained.* K( F& {/ c, f( K& y7 ~
5 v' a V8 Y' m/ d' d. ]Best Wishes," B J7 a. Z! o
Anjana
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: l# L; j5 a8 Z: W# V4 yHaematologica. 2011 Aug 9. [Epub ahead of print]& ]+ _. f. I1 G7 L4 C- F
Durable complete molecular remission of chronic myeloid leukemia following) H0 S* g2 i8 K: r7 z
dasatinib cessation, despite adverse disease features.& {8 F$ F0 e" \* {6 P2 e9 c
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.$ y- B* n. r6 I3 o
Source
# U, d b/ @7 p6 d6 G) cAdelaide, Australia;
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Abstract" d% [" `& N: D( m
Patients with chronic myeloid leukemia, treated with imatinib, who have a
# Q- o0 w0 y. H4 d- s* P+ a6 ~durable complete molecular response might remain in CMR after stopping$ [/ F) T( @6 R- S- y1 {
treatment. Previous reports of patients stopping treatment in complete molecular
' I4 x5 N& \# p- t# uresponse have included only patients with a good response to imatinib. We/ u7 M2 S' s4 E- z+ S# a S
describe three patients with stable complete molecular response on dasatinib# g' N. {/ S# f0 d2 P
treatment following imatinib failure. Two of the three patients remain in: h; f) Q; T# S: c7 \* R
complete molecular response more than 12 months after stopping dasatinib. In
5 m2 N( \* l2 Y6 T0 `4 r/ cthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
! E$ s! O. v. n+ N- f# k% X( jshow that the leukemic clone remains detectable, as we have previously shown in
4 l: K& N# `4 i5 D, {" [; Simatinib-treated patients. Dasatinib-associated immunological phenomena, such as
& G: @5 A. P! u$ lthe emergence of clonal T cell populations, were observed both in one patient
) u9 c# ~: A0 e# r) u* ]$ g* kwho relapsed and in one patient in remission. Our results suggest that the1 {3 u" q" ^) v1 b6 x F9 U; w! }
characteristics of complete molecular response on dasatinib treatment may be
, P0 y6 W, |8 x0 qsimilar to that achieved with imatinib, at least in patients with adverse
8 f% _ O8 t- l1 Q5 X Q. k6 v0 zdisease features.
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