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。
0 u/ ^) i2 J2 {( ~; [ 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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4 C9 ^5 L' p [$ W作者:来自澳大利亚0 A. q0 H3 v' F* O2 Z
来源:Haematologica. 2011.8.9. b& X2 w: R9 L# m" \3 b% \# W% |
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
7 z6 ?' G$ S* a; qtherapies. Here is a report from Australia on 3 patients who went off Sprycel9 s6 i! |9 \# d7 }
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
6 p+ P! F+ T8 T! z" C4 j( A. nremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
' x+ h; X8 ]0 X/ {/ y- n/ Ndoes spike up the immune system so I hope more reports come out on this issue.
% S7 }+ r% q' }: f$ D% N* K$ B- g# Y
The remarkable news about Sprycel cessation is that all 3 patients had failed# z6 H9 v- _% p" }
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
- |7 T9 A* c9 m5 X( |different from the stopping Gleevec trial in France which only targets patients
: D& C8 z9 h% n# mwho have done well on Gleevec.
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$ b7 A% _& J3 d" [" T9 }6 x1 c! `: CHopefully, the doctors will report on a larger study and long-term to see if the
" J2 W$ a$ V; j* u8 q$ U rresponse off Sprycel is sustained.) }* X- v: G1 X5 m" h' `/ R3 x
8 P. l' q3 P1 o: _" m4 pBest Wishes,
) W3 S" ?7 a9 k2 XAnjana6 |5 l% R8 w7 t( W$ K) u' ~
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( ]* ^$ A6 ~/ ~7 b$ h! rHaematologica. 2011 Aug 9. [Epub ahead of print]
- s: W: D* y4 n3 T) ?1 f) M9 SDurable complete molecular remission of chronic myeloid leukemia following% h. i. W0 S+ q, r" [ p$ P* v1 m
dasatinib cessation, despite adverse disease features.
* T/ \2 Y& F+ M1 z% g8 }Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
# \! }3 i; P6 R9 d4 N, ^- FSource
3 i( e4 {4 X* UAdelaide, Australia;" T" |& x( j1 [ ~5 K
! N+ R6 w/ Q' DAbstract
, T, A9 ]# L# m+ w# ]% H0 h6 D3 S0 kPatients with chronic myeloid leukemia, treated with imatinib, who have a) n2 `5 b5 a* \8 \: ]& ?9 ^
durable complete molecular response might remain in CMR after stopping
, v+ U( ^9 f* ?; l" v1 a5 e( E! Ftreatment. Previous reports of patients stopping treatment in complete molecular3 z: ^. p+ O8 _! {6 U) a) [
response have included only patients with a good response to imatinib. We
. a) d' l( m$ b( f. p8 t8 c6 cdescribe three patients with stable complete molecular response on dasatinib
1 V+ h$ O6 V$ Y* p0 Q6 R0 Utreatment following imatinib failure. Two of the three patients remain in
$ k; d' G( q- ~8 Ocomplete molecular response more than 12 months after stopping dasatinib. In
$ c7 d0 _# H) x# a: c& {these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to3 o e* p4 ?& ^# }) M! b
show that the leukemic clone remains detectable, as we have previously shown in
. P8 } N% N- h5 e; O" a" zimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 Z& S8 `0 y% |9 ^6 uthe emergence of clonal T cell populations, were observed both in one patient
) [& G- g! K" ewho relapsed and in one patient in remission. Our results suggest that the/ J3 S% ]; W, J8 Y
characteristics of complete molecular response on dasatinib treatment may be
/ D+ v# v3 o. R5 G- Q, a/ F. x, vsimilar to that achieved with imatinib, at least in patients with adverse
9 D/ |; n* z! X" E2 idisease features.# M6 [6 ?2 r1 M
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