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。5 a6 g3 w( B# n7 r2 | l) v. [! z
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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; ?2 j/ z7 A' E8 H作者:来自澳大利亚
7 a. _, y' m! F来源:Haematologica. 2011.8.9.6 @9 U: H- `0 A2 u9 t! x
Dear Group,6 Y+ f9 }, P% g [
9 t; A, I# v7 O' VSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML$ _# @ @) V9 e, I5 J4 \. `
therapies. Here is a report from Australia on 3 patients who went off Sprycel0 w G4 u1 r6 p2 p- x; j6 H3 g0 Y& ]* e" A
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ G& p/ N: {; premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 A3 Z, x6 u8 @ P( O* Odoes spike up the immune system so I hope more reports come out on this issue.
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, W0 t. t4 K4 Q- a& l6 ?# w2 BThe remarkable news about Sprycel cessation is that all 3 patients had failed
/ u5 ~; x1 V( F( m6 X% b C, Z2 ^Gleevec and Sprycel was their second TKI so they had resistant disease. This is
& v# M7 ~7 `: f& udifferent from the stopping Gleevec trial in France which only targets patients
" j4 b$ G# ?# I! @; hwho have done well on Gleevec.+ F4 i0 X/ j, k2 t C( ]% N) \
1 X/ L2 r, F$ m# FHopefully, the doctors will report on a larger study and long-term to see if the
5 I% p6 i \( h/ g8 nresponse off Sprycel is sustained.
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H9 A0 h* y( B% l0 X; `% EBest Wishes,1 K4 X& n# y/ B s4 I
Anjana
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5 a o9 v. k$ N4 F6 y w5 w" PHaematologica. 2011 Aug 9. [Epub ahead of print]# z$ s( M u: l" @9 N
Durable complete molecular remission of chronic myeloid leukemia following/ Y0 N: `0 U& n% x( P4 `, u: [
dasatinib cessation, despite adverse disease features.
& F! }( t2 p0 S" Q. R# hRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
* m; x, n) X1 a% z8 s* L* n S; jSource5 l9 z0 Z& Z. z1 v! N& Q
Adelaide, Australia;7 ?% T4 m5 [6 s+ c }- x; y
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Abstract
7 `& ` c' E# e" g4 w5 \" KPatients with chronic myeloid leukemia, treated with imatinib, who have a9 p* b) X L$ @5 K3 q3 B
durable complete molecular response might remain in CMR after stopping
9 ]6 O7 t9 J" W1 p% n, U' ]treatment. Previous reports of patients stopping treatment in complete molecular, h$ u4 e$ P7 H$ ]) x ?9 T/ D
response have included only patients with a good response to imatinib. We5 G! f( ]9 A) L! c
describe three patients with stable complete molecular response on dasatinib
1 T9 ^4 M! L+ [1 t0 ~treatment following imatinib failure. Two of the three patients remain in
( j# o6 U+ f! l4 {# {4 Zcomplete molecular response more than 12 months after stopping dasatinib. In
$ s0 ]& V. k' V8 ~; S B2 Uthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
1 y8 {0 |8 X+ Dshow that the leukemic clone remains detectable, as we have previously shown in
' K A5 f) f0 r3 Z6 wimatinib-treated patients. Dasatinib-associated immunological phenomena, such as" r! B% Z" c- y
the emergence of clonal T cell populations, were observed both in one patient
; w7 W! E0 F; X# \/ Twho relapsed and in one patient in remission. Our results suggest that the$ ?& l5 Q" U1 x3 n$ l3 q5 a+ K
characteristics of complete molecular response on dasatinib treatment may be
' X: D0 S4 C; P/ N2 ?: Y( fsimilar to that achieved with imatinib, at least in patients with adverse/ S% Z; e5 c' h# \7 `6 o
disease features.
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