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。
: J5 g( w$ @% Z/ O% C# m 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。6 T) t* v7 o. Z7 M' x1 `2 m2 A
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作者：来自澳大利亚
- K$ i1 A0 t7 L2 s( }1 E3 ]7 R来源：Haematologica. 2011.8.9.: E8 C7 D9 V5 [. N" }: M+ z- N9 R
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML5 j9 z" ^( g$ Q8 _/ \" O
therapies. Here is a report from Australia on 3 patients who went off Sprycel
y) `% P" x( ?% o' O+ Dafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
- b9 |" h1 V0 Z. s% \1 Oremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& S$ \& D M* p0 @3 t9 P' Bdoes spike up the immune system so I hope more reports come out on this issue.7 k) h) | [5 C7 S1 ^
2 k' B$ Z4 D6 @& k0 NThe remarkable news about Sprycel cessation is that all 3 patients had failed
* z% ]) R4 X6 \. U8 o. r# V0 ^0 tGleevec and Sprycel was their second TKI so they had resistant disease. This is9 i2 L4 e$ Q& F Z2 j$ L
different from the stopping Gleevec trial in France which only targets patients+ O, j4 {* D# _1 \4 r7 i
who have done well on Gleevec.6 L% Y( M* s- w0 Z$ {4 [
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Hopefully, the doctors will report on a larger study and long-term to see if the% A* Z. ?( U! n" T8 r h
response off Sprycel is sustained.
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O; B( V. h( |7 K+ R' uBest Wishes,
$ _% z; L: m0 n" ^% MAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]+ C( S6 ^% e* ?) F. K
Durable complete molecular remission of chronic myeloid leukemia following/ o) M ]0 C% i* M% r7 n0 {
dasatinib cessation, despite adverse disease features.9 i) ~- t |- T) W* J, i
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.* \( Y' j/ V$ U! L; s4 L
Source
r' X2 p- y7 ]3 uAdelaide, Australia;$ ^, h- e% N& a! F6 N! {3 H" q
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Abstract- c p1 p: ?# @
Patients with chronic myeloid leukemia, treated with imatinib, who have a' Q* J& H8 x& h8 e
durable complete molecular response might remain in CMR after stopping
/ C" n0 {9 u5 p# M/ e, f9 _# mtreatment. Previous reports of patients stopping treatment in complete molecular
6 {$ Y/ K( v) m+ a$ Cresponse have included only patients with a good response to imatinib. We+ O% V4 e, M: }5 l! i3 v/ k% j
describe three patients with stable complete molecular response on dasatinib+ c9 f7 b+ J o
treatment following imatinib failure. Two of the three patients remain in$ A7 h. A0 s; s+ _- y# C
complete molecular response more than 12 months after stopping dasatinib. In C$ N# _$ J0 J; r2 o4 P
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& m+ d, a* D2 i0 x! i2 n& i
show that the leukemic clone remains detectable, as we have previously shown in
% G) w7 ?- e5 f; Limatinib-treated patients. Dasatinib-associated immunological phenomena, such as
a, o6 M' B* b% s }# Kthe emergence of clonal T cell populations, were observed both in one patient
9 i* D& P2 D1 ^6 N" z! z$ Dwho relapsed and in one patient in remission. Our results suggest that the( n4 T& z! r; c4 s: I V6 `2 {
characteristics of complete molecular response on dasatinib treatment may be
. m; v9 U5 t! ?, Jsimilar to that achieved with imatinib, at least in patients with adverse
6 _% g5 e1 E3 }) C- n2 `& \. Ndisease features.
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