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。
' t: }. T ^- @: S- _1 ?9 y: @ 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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7 {" M% X t6 a) b, l! j: S& P作者:来自澳大利亚
v, r6 ~) \, N来源:Haematologica. 2011.8.9.# y6 V4 [: Z; ^3 D; P& Q4 ]" L
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" f+ d w2 I( k) y: |
therapies. Here is a report from Australia on 3 patients who went off Sprycel
: X* `$ c* @3 }- Nafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients4 y! O# I8 x0 s; p p& z5 d5 E6 D
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 R `; f! @6 g' cdoes spike up the immune system so I hope more reports come out on this issue.) o' P5 E1 y& E7 Y- M6 _
7 U. A& _# f6 B" u) c8 `The remarkable news about Sprycel cessation is that all 3 patients had failed
& x2 ^- N7 s$ F- ^Gleevec and Sprycel was their second TKI so they had resistant disease. This is
- a P% T) j s2 `( [different from the stopping Gleevec trial in France which only targets patients
1 v# u6 o: G( U0 x8 Twho have done well on Gleevec.
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7 s% [1 T( e- R/ u! gHopefully, the doctors will report on a larger study and long-term to see if the/ [0 G9 n- R- |/ D; h! S( m9 ~
response off Sprycel is sustained.
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9 \' S" s& F' ^0 MBest Wishes,& |1 o. K$ h7 G2 h" f; t$ f2 U W
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
, X) j5 ]+ Q; E' A7 P+ UDurable complete molecular remission of chronic myeloid leukemia following
/ n: k! g1 L' s" {- g& ~; ]dasatinib cessation, despite adverse disease features.
- e3 C6 z/ Q1 O! O( CRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.3 c" {$ u! d5 [7 j: N
Source
5 z% [$ x4 S$ k+ p h8 z9 \Adelaide, Australia;
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" K- e/ s2 E* ~9 e8 dAbstract: ?% s+ o( q# U. Q# [ e
Patients with chronic myeloid leukemia, treated with imatinib, who have a
/ o q6 m+ b+ y F/ ]+ V% Bdurable complete molecular response might remain in CMR after stopping7 y. p: }6 X& R1 T
treatment. Previous reports of patients stopping treatment in complete molecular- e# M. r' I6 g4 _5 W
response have included only patients with a good response to imatinib. We
' s+ K. d0 ~0 Z1 n' e5 ^describe three patients with stable complete molecular response on dasatinib
' y( B/ _7 e. W, L6 h. ltreatment following imatinib failure. Two of the three patients remain in
1 Y( u1 e# a6 K3 H7 f1 kcomplete molecular response more than 12 months after stopping dasatinib. In
; v) d1 H3 L6 s" B! athese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to a$ E# r2 A* ?( a6 k1 t6 R
show that the leukemic clone remains detectable, as we have previously shown in* F) Z3 U* A; `- `" N3 u4 V0 _
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as' B; A" ^/ w3 u0 j
the emergence of clonal T cell populations, were observed both in one patient" U3 E y7 j( h
who relapsed and in one patient in remission. Our results suggest that the
8 A! n( [5 z0 ucharacteristics of complete molecular response on dasatinib treatment may be
' Z0 H9 `4 N' rsimilar to that achieved with imatinib, at least in patients with adverse4 v, t0 [3 @& \4 s% d2 m6 _
disease features.
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