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。
4 j: u) H, Q- e; }3 T% h 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
! c; k% J0 [6 P2 d f% k+ k6 s来源：Haematologica. 2011.8.9.. Y) i( D1 Z: z3 g5 u& k: L
Dear Group,
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+ t5 Q! C4 o$ k( z ^5 C7 a! QSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
- N7 l9 @& ?: T7 T. qtherapies. Here is a report from Australia on 3 patients who went off Sprycel
1 m5 O3 n/ O+ n: I9 F9 pafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients! E3 L8 q8 p& X) a& g+ `6 m( j! Z
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel* x6 k7 m' S1 j
does spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed6 y+ i: }9 d. w
Gleevec and Sprycel was their second TKI so they had resistant disease. This is u' B% A6 Z* S) D$ [8 C* x
different from the stopping Gleevec trial in France which only targets patients
5 t* [" g$ G. `/ g+ ^& zwho 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
`) I6 S# B0 Wresponse off Sprycel is sustained./ S7 S6 t& o) J! s& I/ ~( y" N5 } O
2 ]6 S' t0 d$ V' m) ^3 DBest Wishes,6 I1 |6 d' V% ]* T4 d
Anjana" I+ J9 @' W2 h" c
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Haematologica. 2011 Aug 9. [Epub ahead of print]
5 h- |. ~7 o* ?Durable complete molecular remission of chronic myeloid leukemia following
' ^+ ?& Y- p* y: v% l: H) F8 v, Mdasatinib cessation, despite adverse disease features.
/ H6 B) F% H5 d$ Y# s2 l9 F- ~! N" HRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
5 `% C. H6 | @( g" F" [% E7 {Source
& k& c' n1 A3 M# G, U, VAdelaide, Australia;
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Abstract
+ x$ F5 y4 m8 q& BPatients with chronic myeloid leukemia, treated with imatinib, who have a- G- N' e; Q: i4 t( {* \
durable complete molecular response might remain in CMR after stopping
9 {9 p4 H- K% E- o6 U+ I( D0 I6 ?treatment. Previous reports of patients stopping treatment in complete molecular+ I" j- t& |( S) B! z+ A
response have included only patients with a good response to imatinib. We
: i2 K5 \8 ^, |# cdescribe three patients with stable complete molecular response on dasatinib
# ^6 R# D: ^: s. mtreatment following imatinib failure. Two of the three patients remain in
0 W4 @$ }- ]" Bcomplete molecular response more than 12 months after stopping dasatinib. In
. @# F1 Y8 ~1 u' _* {; qthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 _3 m5 }* ^: J- _" L% n, b2 b
show that the leukemic clone remains detectable, as we have previously shown in4 Z2 x) ~9 M" Q9 M9 u' a7 r
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as1 ]! }( v# J6 J$ ]6 r# [
the emergence of clonal T cell populations, were observed both in one patient/ j! q# `' c, t+ f1 h
who relapsed and in one patient in remission. Our results suggest that the
5 G: e1 j9 f( x+ f; K4 C) \% H: Ncharacteristics of complete molecular response on dasatinib treatment may be+ q) b5 \6 z. m0 T$ i
similar to that achieved with imatinib, at least in patients with adverse- _3 y; e/ b5 Z9 l8 ?$ D( ]9 Q
disease features.0 ]+ q% e3 G/ v$ N3 B; N2 X# d& D
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