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。; q' j' w. C* O" R( b) O% 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。
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; d, Q: {: s' d2 B( v$ ^作者:来自澳大利亚# B y+ x1 g% o% r/ ?
来源:Haematologica. 2011.8.9.
1 _# C9 H$ m2 _2 W8 p& dDear Group,
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% I; M |, D1 V8 Y) o! f- U* |9 fSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
8 B; R& D# E0 X2 B& Stherapies. Here is a report from Australia on 3 patients who went off Sprycel3 T6 k9 `4 {$ n) b( w; d' l9 v
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
+ @5 q! I( T" Y4 u {remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( F) C$ y2 {0 J8 {& W5 C
does spike up the immune system so I hope more reports come out on this issue.$ |0 b: y3 s9 Q% s t2 U7 G
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The remarkable news about Sprycel cessation is that all 3 patients had failed
- {4 v$ h d% ~4 U) ]0 HGleevec and Sprycel was their second TKI so they had resistant disease. This is
9 _" R; Z5 Y* x7 m+ p9 I0 R( fdifferent from the stopping Gleevec trial in France which only targets patients% i4 j5 ?1 A, W: I" Y
who have done well on Gleevec.* \$ d# ], K3 G/ Q
. a! ?9 ~# | G, f3 z* E2 j8 EHopefully, the doctors will report on a larger study and long-term to see if the
* L& o+ T- M5 A, K# {response off Sprycel is sustained.) b. D& A# Z1 c5 K+ s( Q5 Z) i
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Best Wishes,7 `, @6 Q& P8 O
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]( M* P0 Y" `8 _7 ]5 W: Y% @, ^1 H1 r
Durable complete molecular remission of chronic myeloid leukemia following
# c! P$ M; I7 `3 `% K9 M6 |7 Wdasatinib cessation, despite adverse disease features.
3 m% f: q( i1 \9 D3 ZRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;
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Abstract
$ O1 ?# c* V9 F( _' aPatients with chronic myeloid leukemia, treated with imatinib, who have a
8 B K+ o e7 B/ i" ]0 [9 Tdurable complete molecular response might remain in CMR after stopping! G4 _4 B$ E, i6 n* J6 c: b8 u
treatment. Previous reports of patients stopping treatment in complete molecular
" a% r6 i; v& B2 X7 d k/ P" eresponse have included only patients with a good response to imatinib. We/ H* M& c7 c: Y% C0 N( O
describe three patients with stable complete molecular response on dasatinib, T% A _3 Q! ?! g" a2 q5 q/ X
treatment following imatinib failure. Two of the three patients remain in
; \9 e; X5 x, I) P, H# |7 [5 f, Lcomplete molecular response more than 12 months after stopping dasatinib. In* ~0 O. Y1 }8 m/ i$ A& b+ \
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, \9 c! U, Y: J& r
show that the leukemic clone remains detectable, as we have previously shown in7 |! N1 _! s9 d% C
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as; H" L5 E9 p* G$ [
the emergence of clonal T cell populations, were observed both in one patient
( j! I/ N4 d7 X( B2 |( w. Ywho relapsed and in one patient in remission. Our results suggest that the' l. V( F, O: c$ d
characteristics of complete molecular response on dasatinib treatment may be: n5 [. J# C6 ?3 W
similar to that achieved with imatinib, at least in patients with adverse
- L& j- G6 b) O7 \1 Jdisease features.
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