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。
' M) T4 K8 i, U5 g! 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。1 K' q- m6 ~7 h3 p, I
# q8 l4 P3 i& @- g/ ^6 C* l( M作者:来自澳大利亚
: V; o' h0 |& x来源:Haematologica. 2011.8.9.9 c! o$ G A8 v7 ] v) b: M6 s5 [
Dear Group,
2 Q1 D/ @( g+ r& {
* c: L4 m; d* j h" D: |; ? z7 e1 aSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML$ G0 s/ g" b; B2 @1 O3 Z4 c
therapies. Here is a report from Australia on 3 patients who went off Sprycel# i% P0 [% J( c Y+ ]6 A! a
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients: \& k4 m1 j6 c& k2 J6 J2 h% n# v
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
P& J' j# ~$ u- Ydoes spike up the immune system so I hope more reports come out on this issue. J! k2 K6 r# n! g$ A
1 q) E- p: Z1 y3 i3 Z( O( g& uThe remarkable news about Sprycel cessation is that all 3 patients had failed
9 W/ [+ \3 A$ l* bGleevec and Sprycel was their second TKI so they had resistant disease. This is3 ]8 M/ n) X' ~
different from the stopping Gleevec trial in France which only targets patients6 M/ _+ t; `/ E @( s
who 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
$ S; W6 S! W6 Y2 K2 B: K3 jresponse off Sprycel is sustained./ X4 k, H) C) [8 ?
! ^6 e6 c% h9 H; W) O& u- \& S2 [5 M
Best Wishes,
" p2 N9 K2 c! I4 mAnjana
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4 K& H5 N" b4 CHaematologica. 2011 Aug 9. [Epub ahead of print]2 m3 x" C* j' c) G ^ ?/ r
Durable complete molecular remission of chronic myeloid leukemia following
# _, V/ g! D: ~- O4 i) m/ Ldasatinib cessation, despite adverse disease features.+ u/ {/ e6 f t9 v% l3 V1 q; x
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
! S8 _2 ?( O& ]9 eSource
- b+ }1 F" q. ~$ kAdelaide, Australia;
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: j' n4 y0 w5 P, U1 q( @/ ZAbstract/ A( p$ ^2 Y! Z2 ^# C+ S5 Y
Patients with chronic myeloid leukemia, treated with imatinib, who have a
- X. H/ Q3 t: [2 S/ M |' Vdurable complete molecular response might remain in CMR after stopping
, O7 v0 i/ Z2 F. q4 Vtreatment. Previous reports of patients stopping treatment in complete molecular
% D& z2 k y4 g: A2 ~9 ]. qresponse have included only patients with a good response to imatinib. We
- y% H4 l% R0 w. F# u* ~describe three patients with stable complete molecular response on dasatinib5 k1 t1 n& r/ ~7 b. J
treatment following imatinib failure. Two of the three patients remain in+ c. ~- ]6 | J! z6 q$ s$ {" Q
complete molecular response more than 12 months after stopping dasatinib. In- R B4 ?# S! {$ \$ K
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* ]# Q4 {( o% {! q$ w+ k; wshow that the leukemic clone remains detectable, as we have previously shown in
% ]* I: j% d3 oimatinib-treated patients. Dasatinib-associated immunological phenomena, such as5 K, U. T! g. n' G8 V
the emergence of clonal T cell populations, were observed both in one patient
5 A6 M% u9 {3 a# B2 dwho relapsed and in one patient in remission. Our results suggest that the
. S" n- w% ~8 E) ?2 y T. A rcharacteristics of complete molecular response on dasatinib treatment may be
% i( M- w- l6 {1 T. r- h& h1 asimilar to that achieved with imatinib, at least in patients with adverse) Z% |& p2 E* Q* f8 e
disease features.) r9 f! f" C/ T3 f- u; S
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