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 e" b( x8 t% Z' d+ Y 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。% X2 f. J1 U9 H6 i/ V. c* P
* G! I6 b% r3 V作者：来自澳大利亚
% @7 N3 i4 Q+ N' W6 K5 O来源：Haematologica. 2011.8.9.5 R- X* a4 r) U T1 p# _; J
Dear Group,
1 r% k7 T- U+ z+ ]: C; y
9 M" ?5 D, ^, M% E5 KSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
# r: [: d! Y8 a4 H$ T) a) ktherapies. Here is a report from Australia on 3 patients who went off Sprycel
' F' M3 `6 ~" k3 f% N( Eafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients P1 h3 F5 V9 ]' a- s
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
3 U* U& k, q# O, w: c' v$ mdoes spike up the immune system so I hope more reports come out on this issue.' q# }1 H/ ?- L8 G% \7 P) B' |4 n: F
; w. ?* S% X5 N# z3 xThe remarkable news about Sprycel cessation is that all 3 patients had failed
# @! P4 Z+ q+ t6 m8 z$ vGleevec and Sprycel was their second TKI so they had resistant disease. This is# M' p5 z( P! e: V0 \. X: T/ D
different from the stopping Gleevec trial in France which only targets patients: l/ S E- ~; l' X
who have done well on Gleevec.
( o3 U; D. _2 y" g7 d
% l# s4 s% j+ JHopefully, the doctors will report on a larger study and long-term to see if the" x/ u5 E* B& D7 x s, n
response off Sprycel is sustained.
9 s: L7 L, y; V& h: I' |5 V8 W# I. v
Best Wishes,
$ G+ H% J. O. m/ ?Anjana; f3 z" T& u& k$ @" V* ]9 m4 a
4 [! v1 W: U/ X3 X
# x0 W3 ~; j7 {
! v9 T# \ s7 l9 N& x/ HHaematologica. 2011 Aug 9. [Epub ahead of print]& V' E! Y: H7 ~0 P$ |
Durable complete molecular remission of chronic myeloid leukemia following: K: S. Q0 r8 ^9 l a$ R" l
dasatinib cessation, despite adverse disease features.3 r' z- V P) X) y# \
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.3 Q+ z8 ?4 r/ T1 c) j) r- b4 }7 D
Source! m' H2 r/ P1 u
Adelaide, Australia;
$ M1 P% B( {& F/ [! R$ u$ s5 r& F, \3 h% |* i
Abstract& S7 }6 K! X, u( `1 ]8 e
Patients with chronic myeloid leukemia, treated with imatinib, who have a: s" ]. D2 r0 k) c. @7 \- p9 P
durable complete molecular response might remain in CMR after stopping" i0 w% m# z/ D/ s. B; i) h
treatment. Previous reports of patients stopping treatment in complete molecular
% l/ [- H. Q9 c2 @; }response have included only patients with a good response to imatinib. We
/ y+ ^4 n- c" t5 idescribe three patients with stable complete molecular response on dasatinib
/ a. p0 A) V y/ M3 qtreatment following imatinib failure. Two of the three patients remain in! ], a9 l* E$ \# ~* s$ }
complete molecular response more than 12 months after stopping dasatinib. In
- ^2 \( ]- B, o0 ?5 Cthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to; m" f' |+ m. x6 ?" f" G( H
show that the leukemic clone remains detectable, as we have previously shown in4 u D8 d! `% K P- O2 Y
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as; y& b, F; H$ K3 X: C1 R
the emergence of clonal T cell populations, were observed both in one patient9 u$ ~. C6 H* j! r
who relapsed and in one patient in remission. Our results suggest that the9 b3 y- ?# F9 ^$ o) ^+ o l3 N; Z
characteristics of complete molecular response on dasatinib treatment may be
0 q Q. e4 p, x1 O0 \! Osimilar to that achieved with imatinib, at least in patients with adverse0 i- \ R: @1 \1 d# G
disease features./ \- o! l1 k) P- ^9 @
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