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。
, X9 m/ e% g% Q" A' A# Q5 I 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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作者:来自澳大利亚
8 D5 S7 L' M K/ v9 Q$ K" W来源:Haematologica. 2011.8.9.
7 B* _; y: H6 {3 vDear Group,- c6 n$ a4 u0 Z# ?3 e C1 c6 h
2 g1 N# c3 X) E0 H' ~Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ d$ w1 ~2 S$ ]+ }/ w' P" T9 ?0 y
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 q) y# y2 V! d4 }0 o
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ z/ j+ f0 X. {remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
6 I( H% w1 i) Ldoes spike up the immune system so I hope more reports come out on this issue.
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j8 [( X* v3 w1 MThe remarkable news about Sprycel cessation is that all 3 patients had failed9 w2 z* q8 M" g7 m' c# J( z
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
" u; S$ O! h" ~3 N% Fdifferent from the stopping Gleevec trial in France which only targets patients
% h" O! @4 k' S6 i" F+ uwho have done well on Gleevec.
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3 Z: B) e7 P1 @. W. v, oHopefully, the doctors will report on a larger study and long-term to see if the
7 I% l, N, d) Q4 o. L+ q; J+ c Aresponse off Sprycel is sustained.
7 X, z" O8 R4 |! D: V: i: W2 ]
: @$ Q9 l/ i; U9 DBest Wishes,
& h5 q8 S4 Y# H( r2 R7 t0 qAnjana) y% y5 @' j9 l1 p! n% H
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; t- a7 R( r8 u1 B! h& l1 XHaematologica. 2011 Aug 9. [Epub ahead of print]9 O, b* j% [/ n. L( V/ E& n& i
Durable complete molecular remission of chronic myeloid leukemia following
* \) _! T) {" Y- }- u( \dasatinib cessation, despite adverse disease features.+ M+ T# j) C2 ?' X% J( O+ w
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
- U( Y" v& n& g* X9 P0 ~Source! q- k" Q6 m/ H
Adelaide, Australia;3 w$ i N, x3 m! @9 S2 J
8 }( \& Q0 s2 q. X5 O4 o, w' HAbstract9 Q m$ C9 X- E( W; D; o9 K
Patients with chronic myeloid leukemia, treated with imatinib, who have a; r/ t3 }6 N4 }! x y
durable complete molecular response might remain in CMR after stopping$ {6 | G( @/ F/ ?/ A( M$ m: ]- Q
treatment. Previous reports of patients stopping treatment in complete molecular! A9 G- t5 M( D& r6 D- l$ h6 X
response have included only patients with a good response to imatinib. We: V+ B+ [) a& H* J v
describe three patients with stable complete molecular response on dasatinib
/ f) o: W+ E9 }& @+ C4 o6 W% atreatment following imatinib failure. Two of the three patients remain in
# A! F! o o% v: t( v3 }& p/ gcomplete molecular response more than 12 months after stopping dasatinib. In
% v% {5 C/ i) Q gthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to! c6 F6 t& }2 f1 V
show that the leukemic clone remains detectable, as we have previously shown in
. W {+ ^: S+ v0 Q; U. Nimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
' L1 H2 U* h8 Y4 R& T6 ^the emergence of clonal T cell populations, were observed both in one patient
n3 L5 _- F N& W/ r8 G$ Fwho relapsed and in one patient in remission. Our results suggest that the& e& P! m& ^+ R+ }( X
characteristics of complete molecular response on dasatinib treatment may be
+ [ q1 c6 f/ v& C* osimilar to that achieved with imatinib, at least in patients with adverse
& Y& M! |& C0 \' y+ g4 ~disease features.4 }* V( ]4 W; {
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