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。% A$ D* j; k/ ?/ o# a% J
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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( s# e6 t$ ^2 N6 n5 V l g% V作者:来自澳大利亚- v* Y% Y! i1 p/ z! I' R5 s2 p
来源:Haematologica. 2011.8.9., P! v2 _: P( A( @
Dear Group,# N( T2 z7 p& L8 e& I8 j
% Y3 M0 r; |9 X7 } MSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
6 C+ d" u0 ?9 D" etherapies. Here is a report from Australia on 3 patients who went off Sprycel/ ?% U. L6 d( d3 X1 k7 A& g
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
' q& W2 Y7 K$ A8 Lremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( f3 w1 J8 X, v! q h4 ]4 k2 J
does spike up the immune system so I hope more reports come out on this issue.; u% [' _' M( d
$ M& e9 y0 [- ?( g6 a' Z) HThe remarkable news about Sprycel cessation is that all 3 patients had failed) Y; N& @, M) \3 ~ o, d- t2 Z
Gleevec and Sprycel was their second TKI so they had resistant disease. This is" C$ M; @' S# U+ m
different from the stopping Gleevec trial in France which only targets patients
% ^9 e& b1 d* \4 Z' zwho have done well on Gleevec./ F% u" g# v2 K7 B. f1 ?$ e
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Hopefully, the doctors will report on a larger study and long-term to see if the
6 ^3 ]4 I/ F& wresponse off Sprycel is sustained.. m0 x; m+ e. K8 T1 x! V7 r
4 W- c0 Y. Q. V( a& a7 t* vBest Wishes, S1 b; K, y Y. C, r
Anjana
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( b; h! O- A# r. q) S4 EHaematologica. 2011 Aug 9. [Epub ahead of print]
" }6 b3 v2 _% f" E, o6 v$ ]. KDurable complete molecular remission of chronic myeloid leukemia following7 j1 |+ H) n A9 y5 }; i. E( V
dasatinib cessation, despite adverse disease features.! r j9 r" k/ ]7 Q6 ?- r
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 `* I0 P3 U' ?) n2 r% q
Source
; x& b- ?7 H0 T# j* ^5 R0 m2 @: BAdelaide, Australia;
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6 T5 s4 x9 N$ F# U0 S+ ?1 n8 CAbstract
5 m: Y+ b% r+ T# N, uPatients with chronic myeloid leukemia, treated with imatinib, who have a$ E! _5 Z$ J$ ]. Y% H% R
durable complete molecular response might remain in CMR after stopping P/ i( [# C7 D+ f$ }6 H3 O
treatment. Previous reports of patients stopping treatment in complete molecular/ y5 \, ?# _! p9 A/ C4 I5 d5 G
response have included only patients with a good response to imatinib. We* h* \: ^% ^& s6 S
describe three patients with stable complete molecular response on dasatinib" F6 [/ D+ g2 B- v! F m0 f. G" U7 c
treatment following imatinib failure. Two of the three patients remain in) G0 }" U% `- Z1 Z7 b! x
complete molecular response more than 12 months after stopping dasatinib. In9 q8 Z" f- A# g# S9 e
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to: p, N' |% _2 v$ e/ G2 b3 F
show that the leukemic clone remains detectable, as we have previously shown in
) [+ v7 h6 T" j3 z" y, oimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
5 W& Q; u6 M& ^, l, z6 |5 x! [the emergence of clonal T cell populations, were observed both in one patient* H4 u! w; `' f6 h; C' o1 t
who relapsed and in one patient in remission. Our results suggest that the" Z! j$ A8 Q- |/ ?9 K/ C
characteristics of complete molecular response on dasatinib treatment may be9 Y2 H2 M/ u9 ^$ }. d
similar to that achieved with imatinib, at least in patients with adverse
4 k9 l! d1 R l9 mdisease features.( Y9 [' `% y; t
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