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+ t% ^( ~! }1 n" C/ D9 Q
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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作者:来自澳大利亚
4 f; R# K" k, G* F来源:Haematologica. 2011.8.9.1 y" N l4 p; h! B) Z1 k# k T) g
Dear Group,
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& Y0 c5 S# ?" ?, W; Q6 n: [5 V4 u. ^Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML, t2 C1 u/ W. Y0 `
therapies. Here is a report from Australia on 3 patients who went off Sprycel
/ n2 D. M1 F: `8 X& L5 B( s4 Qafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
: E& b: e: c/ d2 Z! `0 M F' a9 Tremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel* \4 h* t& u5 n+ E/ Y' l1 b6 K* T
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
6 e/ x, F" Z/ d' {/ x3 L/ K3 j% dGleevec and Sprycel was their second TKI so they had resistant disease. This is
& x: l/ x4 p1 O1 N" f. Zdifferent from the stopping Gleevec trial in France which only targets patients
0 R1 K4 L' R$ z" }- Iwho have done well on Gleevec.
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* A% k! M, ^. X8 l* B! K( rHopefully, the doctors will report on a larger study and long-term to see if the0 c! R6 y7 V7 N6 R0 C
response off Sprycel is sustained.
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Best Wishes,
: g6 K+ w/ F, X: O8 {3 w: FAnjana
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9 ]# }1 x/ G9 j5 q0 A1 {Haematologica. 2011 Aug 9. [Epub ahead of print]# ~: Q- ]; D* f$ V
Durable complete molecular remission of chronic myeloid leukemia following1 K% q7 x8 ~/ d( M4 G. t
dasatinib cessation, despite adverse disease features.; R. s0 N: s |" W& s% o. @* @: L* O
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
) \0 ]: [0 w6 ?+ c; X# P( WSource
/ r# J8 G6 r0 |/ j& [Adelaide, Australia;0 a: `* S5 h# t$ e, V. E# ?2 ?% n/ ?# Z
5 I: C4 H; ?& ~- y( l4 B" [& A2 u, {
Abstract
5 [/ T6 p& ^: B5 {9 u% {: _Patients with chronic myeloid leukemia, treated with imatinib, who have a6 J: v8 I% _, U6 k% `! f
durable complete molecular response might remain in CMR after stopping/ C- t, R4 p N7 W y! Z+ H# X
treatment. Previous reports of patients stopping treatment in complete molecular0 E* O/ {! ~& w: X% q2 y4 w
response have included only patients with a good response to imatinib. We
" R# Z% W4 t( i1 v7 l# X7 ~describe three patients with stable complete molecular response on dasatinib
+ {' E3 N& |( ftreatment following imatinib failure. Two of the three patients remain in
' U7 N9 [1 \# a) ]5 Ncomplete molecular response more than 12 months after stopping dasatinib. In" @6 R" d6 o. [- g T, U
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ p# D, p* b# r- D
show that the leukemic clone remains detectable, as we have previously shown in
$ j' V8 x" I2 b* L( W2 X* O7 uimatinib-treated patients. Dasatinib-associated immunological phenomena, such as" Q0 I3 U! q/ M# T2 }# I% d; d
the emergence of clonal T cell populations, were observed both in one patient
$ V' [' i3 K _) `6 ~3 swho relapsed and in one patient in remission. Our results suggest that the
) U' G: h" P- n* @: G% x5 I8 h# xcharacteristics of complete molecular response on dasatinib treatment may be
) N# o- o8 x1 R) ~; p5 O2 ssimilar to that achieved with imatinib, at least in patients with adverse
) T7 j5 K! L" `' Y. ldisease features.
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