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。
+ w; }* H3 ` Y# t 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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1 y9 |- h) L! c8 s作者：来自澳大利亚, S) j6 [( f# h' a; |( i% y @
来源：Haematologica. 2011.8.9.
( a: t8 q6 d0 ]Dear Group,' v& B$ A. w' F* E% p# l/ x6 G
+ A( [, E. B8 BSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML- t( F! C' Y2 @9 B* }+ J7 x: t
therapies. Here is a report from Australia on 3 patients who went off Sprycel2 g5 Y, H$ i: G' V3 c" ]: S
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients* v/ x+ h! j# G6 v5 q8 s
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( `2 z, P5 p7 S# l' L1 D% b! |7 F
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 failed
9 m! ?7 L [7 c5 R. I. OGleevec and Sprycel was their second TKI so they had resistant disease. This is9 N# ~% M, ~& o1 ?
different from the stopping Gleevec trial in France which only targets patients- ~: k2 B& y/ L1 R5 G$ {
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 the1 g5 D4 ^- v0 c; @! W. D$ K: _
response off Sprycel is sustained.
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4 ~ w4 {& [% I. P% x7 A3 T7 YBest Wishes,7 [* M9 j4 Z0 D4 E
Anjana! r0 T, E* G" m
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. x! T- i0 P }' Z6 ]Haematologica. 2011 Aug 9. [Epub ahead of print]4 y2 C! ?+ {; b4 ]( x. r/ o6 _
Durable complete molecular remission of chronic myeloid leukemia following- r3 G; F7 S1 H
dasatinib cessation, despite adverse disease features.
5 R9 E7 Q3 z9 V6 xRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.7 M5 F, I3 m( T+ O5 Y% P
Source
" J2 @. Y: f" F/ `- bAdelaide, Australia;% b' f" A! K3 S; E& B7 U# q- P9 @
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Patients with chronic myeloid leukemia, treated with imatinib, who have a
+ Y0 O& M7 e6 }" `5 \- zdurable complete molecular response might remain in CMR after stopping
7 N3 W4 r, m J M) ltreatment. Previous reports of patients stopping treatment in complete molecular
* X) |4 N4 ^- A# N6 q. mresponse have included only patients with a good response to imatinib. We
$ r2 i) x! M6 pdescribe three patients with stable complete molecular response on dasatinib
3 X/ m0 Z* _% n0 S. v7 Utreatment following imatinib failure. Two of the three patients remain in
7 E2 n1 F- }' I! ?4 Fcomplete molecular response more than 12 months after stopping dasatinib. In
# i2 P2 u! }4 Y' U, p3 lthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
. X" w. l7 z% M5 j2 ^: \: vshow that the leukemic clone remains detectable, as we have previously shown in
8 t, f9 c- ~) b' f9 `imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- s& G" ]% W; _& s+ b$ k+ d& s
the emergence of clonal T cell populations, were observed both in one patient
6 F6 m; q' q3 p, ` @/ D+ bwho relapsed and in one patient in remission. Our results suggest that the2 X4 P! \! n6 J9 J4 Q5 E [
characteristics of complete molecular response on dasatinib treatment may be2 G$ |5 u# P; _9 ~$ O+ E! f+ i
similar to that achieved with imatinib, at least in patients with adverse; J! w: m- U" p1 P4 ~
disease features.
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