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。3 t [1 c/ t( J8 y) P+ j$ K
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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( H# R; m0 J/ H4 T; v作者：来自澳大利亚
L* @ @ m( Y$ s& L来源：Haematologica. 2011.8.9. O; R% `/ r' x0 U4 q) P* m
Dear Group,, b% I: R! X. M2 l& p- [
# p1 m: a+ p; i) bSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
. ]8 r' N! v" [1 H) r& a( `4 [therapies. Here is a report from Australia on 3 patients who went off Sprycel
+ ^. f' |, G: i: D+ Y1 L( Hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
. v% |( {5 l" ?3 z4 Eremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel: l4 o& d( L b. Z
does spike up the immune system so I hope more reports come out on this issue.: H U, j& H- Z D$ {
, n3 d: ^) B# r+ M, W1 [
The remarkable news about Sprycel cessation is that all 3 patients had failed
" D# ]* Q' p* {6 y7 G: sGleevec and Sprycel was their second TKI so they had resistant disease. This is
/ ?; S N( S, z. ]different from the stopping Gleevec trial in France which only targets patients
% m3 S6 V/ _* A7 s1 Lwho have done well on Gleevec.9 E8 P, a6 Z- m
1 }) Y/ |6 j! b& l- pHopefully, the doctors will report on a larger study and long-term to see if the
0 h4 u; `# G7 ?4 X! }3 ^response off Sprycel is sustained.
k+ {, s. u; v+ }/ V8 V( `
7 l# [# o3 I- s! ~; i4 QBest Wishes,
4 }! \' _( h' ^4 qAnjana) j2 ^/ K& T& j* N s& J7 ~
9 f- p, z0 [$ Y" N; p2 |; U
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Haematologica. 2011 Aug 9. [Epub ahead of print]! M- {2 q/ H$ f* [4 s- s8 e/ _. Z
Durable complete molecular remission of chronic myeloid leukemia following
+ w4 j o' o, [* Y6 z! d: Fdasatinib cessation, despite adverse disease features.
" i) m4 @" N( q$ M; JRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( y V- A4 S; B# {) i
Source. I/ E9 Q( l! }: o+ ]" G& E
Adelaide, Australia;& D' T: f- V, \0 g
; i0 W- S+ \4 d
Abstract# j1 L# |6 I1 s- {
Patients with chronic myeloid leukemia, treated with imatinib, who have a3 j. r- O7 w' ^6 `; n T
durable complete molecular response might remain in CMR after stopping# J d/ d: n/ w8 i/ l p5 i# Y
treatment. Previous reports of patients stopping treatment in complete molecular7 _" h6 h I) V+ ?7 C9 B- F5 Y* d
response have included only patients with a good response to imatinib. We& `' K5 U, k1 n/ `) O
describe three patients with stable complete molecular response on dasatinib+ ^' T0 ~! Z7 l$ h, Y6 u$ Q& G
treatment following imatinib failure. Two of the three patients remain in2 X" I* W* v. O# g* P$ p
complete molecular response more than 12 months after stopping dasatinib. In
b V7 D# E; t- I6 i- {; |, [these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to9 o) S# r% m, F0 j; S
show that the leukemic clone remains detectable, as we have previously shown in
: Q, k d/ @; I. M: V, w& Timatinib-treated patients. Dasatinib-associated immunological phenomena, such as+ r" y* }) r, i; S- v K( q
the emergence of clonal T cell populations, were observed both in one patient
, V+ i% Y# M# A' G) }who relapsed and in one patient in remission. Our results suggest that the
: n& h5 c. t% Rcharacteristics of complete molecular response on dasatinib treatment may be" Z7 t' o* G- K
similar to that achieved with imatinib, at least in patients with adverse- |; n3 v* a; c5 X) O
disease features.: U% q# b3 b2 C% U7 p" E
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