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 K8 r7 T( m' ~# T n 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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$ ?9 X3 C# R O' {* ?8 [# @; ~$ @9 Z作者：来自澳大利亚4 b& \ A6 u }( K6 R' e2 f( K
来源：Haematologica. 2011.8.9.- [7 B4 I' \- J4 B
Dear Group,
7 C" S* r& p/ d3 N6 Q! }- |. A$ C3 V3 G+ o. Y. o
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
* u% M+ f, W, J6 _( B% T' O& Xtherapies. Here is a report from Australia on 3 patients who went off Sprycel" h( t1 I5 T! y4 ?- @; G
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients0 `* J+ `& _1 \, t% r9 ~
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
! U# U1 I3 N; O( G, J, N J) H, rdoes spike up the immune system so I hope more reports come out on this issue.3 @4 s0 w; ~7 T! E
& R6 d$ `2 X1 i% i* O5 o dThe remarkable news about Sprycel cessation is that all 3 patients had failed$ |" X9 l; U" n% ? W
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
' D8 q% ?8 u7 z$ H: ^different from the stopping Gleevec trial in France which only targets patients
3 B/ k8 T7 x6 k$ N3 b$ {# \who have done well on Gleevec.
3 H" I9 f" x% g ]& B' C1 Q( c4 @1 V2 D$ K0 F' H9 _; V
Hopefully, the doctors will report on a larger study and long-term to see if the
, B+ h) t0 V" W1 x) Yresponse off Sprycel is sustained.- G0 C S2 \4 g8 l/ i
+ A e& I- i) L4 N: ?6 Y" ]8 Y" m9 V
Best Wishes,
2 {" D. t$ Y1 f$ Z. K) o* uAnjana
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1 F% ^# u& H* ^2 RHaematologica. 2011 Aug 9. [Epub ahead of print]9 Q0 E; ~. e. n, D3 ]7 _
Durable complete molecular remission of chronic myeloid leukemia following
$ h* Y* ^2 }1 K! ^3 q+ j+ @dasatinib cessation, despite adverse disease features.! x6 J, I/ X( r) C" X: ~! y" q V
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' {( O' R9 t6 r, K$ X+ g9 R
Source
+ p1 ~0 D3 P' e) v! {4 E+ gAdelaide, Australia;
" O2 S* `2 r- n4 \6 w8 O7 q0 E8 `- V: H& x
Abstract
9 ^/ M+ B- ]. H; W6 vPatients with chronic myeloid leukemia, treated with imatinib, who have a
8 O9 n$ w+ O" g5 A6 s( [* Kdurable complete molecular response might remain in CMR after stopping+ U) i8 D, V) M+ p
treatment. Previous reports of patients stopping treatment in complete molecular
4 j. W/ f3 ?2 t, q: ^- e4 D- \response have included only patients with a good response to imatinib. We
1 G8 T* f9 P: U$ P1 y* @- m5 rdescribe three patients with stable complete molecular response on dasatinib
* E/ `1 X- j; ?' l" u1 j$ v# btreatment following imatinib failure. Two of the three patients remain in
6 {! H" r/ Z5 A: X, Kcomplete molecular response more than 12 months after stopping dasatinib. In
- h4 e1 B$ R0 \ ?0 D" pthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) h, X6 M7 D0 @/ }6 X4 o) Eshow that the leukemic clone remains detectable, as we have previously shown in
" b( g. O, W1 [6 r+ T" uimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
; x* i p3 v0 B% v: y& v8 hthe emergence of clonal T cell populations, were observed both in one patient
# o9 P0 R$ Q8 A" U# Gwho relapsed and in one patient in remission. Our results suggest that the
6 L; Y l5 w( |9 Kcharacteristics of complete molecular response on dasatinib treatment may be- D8 M5 ]3 y( J9 o3 w8 H* w6 e/ R: Q
similar to that achieved with imatinib, at least in patients with adverse& l9 C* k! L( m( O$ g9 f5 ]+ ]
disease features.5 l0 e5 D" t( G4 A, Y
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