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。/ U0 c) I- J- @# I# s9 c4 J7 c5 H
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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+ ^: u3 v) [* F! n作者:来自澳大利亚
r- s3 Q6 J7 E1 x' H' k& H来源:Haematologica. 2011.8.9./ | z' U( C" u' }. o
Dear Group," H; `2 g3 f' Q, @ b# `2 Q
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML% C" }: e7 q6 ~5 C- }0 p" {
therapies. Here is a report from Australia on 3 patients who went off Sprycel9 _" B K+ v( X- }: ]3 K- E
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients. _6 [1 E) Q7 ]; U9 E& @
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
/ H5 m, c1 l; S9 x9 D0 sdoes 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
5 a- J4 A# N6 CGleevec and Sprycel was their second TKI so they had resistant disease. This is1 D! u, {( [; H: r( E7 L
different from the stopping Gleevec trial in France which only targets patients
* y: p l" B4 Z0 S# G, A# Fwho have done well on Gleevec.
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/ c, U- `: N }- C) WHopefully, the doctors will report on a larger study and long-term to see if the9 X7 R* }$ D* g4 S; X' _) {% K
response off Sprycel is sustained.8 F8 x. M+ R- G0 v* D" Y% o
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Best Wishes,5 M( z2 Y2 F# m0 L
Anjana( E! I- z8 m$ C
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- o4 w- m2 u+ p, L3 }9 YHaematologica. 2011 Aug 9. [Epub ahead of print]* r- e! t8 ~% g7 T* q
Durable complete molecular remission of chronic myeloid leukemia following
% Q$ l1 O3 W/ j' ^( }dasatinib cessation, despite adverse disease features.6 x9 j* _4 b" Q5 w+ a
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP. h! l# t6 l9 m9 ]; W' o
Source; P- n' W& y) S4 k* p' m
Adelaide, Australia;0 a H. J; T3 F: X9 u
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Abstract
/ l( {' X4 S$ _5 ]% p: m9 fPatients with chronic myeloid leukemia, treated with imatinib, who have a8 q v3 O9 ^3 ]! B; w& W" U [
durable complete molecular response might remain in CMR after stopping4 M+ N8 S; ?) d% @1 M
treatment. Previous reports of patients stopping treatment in complete molecular
/ `- j; K( ~0 ^; h6 Zresponse have included only patients with a good response to imatinib. We: D$ X2 a8 t# V1 }; z s
describe three patients with stable complete molecular response on dasatinib* X' r' X1 y; F: n* R" U
treatment following imatinib failure. Two of the three patients remain in
; g# |/ e* u# o# Ycomplete molecular response more than 12 months after stopping dasatinib. In
5 A E- d& B9 S) p( cthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to3 n3 X" J8 U6 A% p
show that the leukemic clone remains detectable, as we have previously shown in" C8 l0 b! X, }% C5 ~
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as9 p8 L0 m$ @/ n, ^& v! l
the emergence of clonal T cell populations, were observed both in one patient$ N" _1 P; o: I7 B
who relapsed and in one patient in remission. Our results suggest that the3 V1 S% @5 ~+ S2 l |
characteristics of complete molecular response on dasatinib treatment may be
1 m1 D( @% {/ ~/ h* J0 J' z' K- q4 ~similar to that achieved with imatinib, at least in patients with adverse
, L6 w. |4 V& C7 `) v6 Gdisease features.
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