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。
: A. j& s0 X+ Q" q3 E' 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。. B' i5 E8 |+ r
' p) K# ^0 s$ g% ]! i* R& j( B作者:来自澳大利亚
$ D, u& n% T* K0 p来源:Haematologica. 2011.8.9.
" G& a$ r2 s3 jDear Group,2 { O/ i0 E( p$ q5 b2 N" ]$ K3 I" }
- M. m- c' L5 a5 ^/ z1 zSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: t$ ^& P- N! @- n. Dtherapies. Here is a report from Australia on 3 patients who went off Sprycel' Q; q0 }$ A9 b7 s7 b) r
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
7 t. _$ b. Z5 Y. p' o* b* @remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel9 A7 t: |; e8 H
does spike up the immune system so I hope more reports come out on this issue.7 c2 i3 K! P t( {% k) Q
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The remarkable news about Sprycel cessation is that all 3 patients had failed
& Y) z [3 S! D( WGleevec and Sprycel was their second TKI so they had resistant disease. This is- Q {! W7 i! I w" D+ M
different from the stopping Gleevec trial in France which only targets patients, `; z0 G5 e* e: B- d; [
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
# M' }$ d4 @1 B8 k/ jresponse off Sprycel is sustained.; i' k$ n; [ q+ Y c* x
: a: R/ B3 z7 y/ LBest Wishes,8 \6 |2 u+ Q+ Q4 ^8 l* p1 |
Anjana$ B" F* G: m( T- O1 \3 o# @# }
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+ l2 q, h: o# E+ ?
# f2 h0 D0 w: I$ K& KHaematologica. 2011 Aug 9. [Epub ahead of print]
1 b" f; S: b6 \" F3 s w QDurable complete molecular remission of chronic myeloid leukemia following L$ O- ~" P" r! `- J
dasatinib cessation, despite adverse disease features.
7 ^. F. ^5 D. a- m& aRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
5 Z% G' }7 `; M+ e6 x; A1 ISource
4 P) B2 ]4 ?7 ]Adelaide, Australia;) p" Y! U+ |. {' m0 S3 o9 E: N p
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Abstract, H0 c5 j: x3 s& b* `" n( G
Patients with chronic myeloid leukemia, treated with imatinib, who have a6 M" @4 I8 u" l( X5 D# S/ b
durable complete molecular response might remain in CMR after stopping
7 w/ d. o: U+ _9 Z* t' |treatment. Previous reports of patients stopping treatment in complete molecular3 |8 O9 ^+ F" C: V' S
response have included only patients with a good response to imatinib. We6 p4 t6 C# s# y, t) Q3 y
describe three patients with stable complete molecular response on dasatinib- _% i. t7 l1 U+ f
treatment following imatinib failure. Two of the three patients remain in8 [" S/ s$ i! J+ R: |2 v* X
complete molecular response more than 12 months after stopping dasatinib. In( I9 U2 @- U: z! @3 Q
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 R" e( z+ ^9 ]! t% S/ Q* H9 b
show that the leukemic clone remains detectable, as we have previously shown in8 X! k* M0 Z; }/ s4 U0 r: `" [- t1 Q
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
. `7 q+ a) Y1 h Ethe emergence of clonal T cell populations, were observed both in one patient
( C+ o) R2 A/ v- a* gwho relapsed and in one patient in remission. Our results suggest that the) g2 K+ F2 O8 n" J3 X
characteristics of complete molecular response on dasatinib treatment may be7 p, d2 D0 F U; L# e
similar to that achieved with imatinib, at least in patients with adverse0 ]' u5 P$ f* u1 b3 y8 j4 ^
disease features.
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