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。) l6 x( z5 b- q1 B5 ~/ Q' u% m3 u# p
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
1 c# v0 s y1 d/ t S来源:Haematologica. 2011.8.9.
. S6 Z* h& p3 L @Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
' t/ K6 B5 K; D' }; S, Ctherapies. Here is a report from Australia on 3 patients who went off Sprycel
% D7 O$ B8 M0 m. {- dafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients0 @- S) m) h# }; L6 L8 s( D
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
: A f( i6 l0 K$ ~/ x$ {" jdoes 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
" _# o7 ?+ ]8 W( V) W, B: s* fGleevec and Sprycel was their second TKI so they had resistant disease. This is
! X8 C7 @) }" R- ^6 t8 N/ J+ I; mdifferent from the stopping Gleevec trial in France which only targets patients3 ~) O: w* Z; I7 z. b3 G8 o
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the% e1 ^5 _5 a5 V. O9 c
response off Sprycel is sustained.0 p7 k; G% B5 I# _1 q4 V
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Best Wishes,- P% R* m3 C! s2 E0 I7 P
Anjana l3 s1 K7 L7 M8 T9 o, ]
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Haematologica. 2011 Aug 9. [Epub ahead of print]5 e _% r. d: d; f2 c
Durable complete molecular remission of chronic myeloid leukemia following
4 }% B: D$ C4 @8 idasatinib cessation, despite adverse disease features.
+ E9 l3 t8 J0 n' s8 A* q( Q. P8 VRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.$ p. ]4 p6 W; m, T. \
Source# c9 U) Z) b- P+ b- x/ V: F$ e& ^
Adelaide, Australia;7 X1 h# m, t, |% f' k& `+ [6 _; W
2 s5 C1 H* }. x4 S8 a- P; z) R0 SAbstract) S7 f# _% N: a; w$ {' P T
Patients with chronic myeloid leukemia, treated with imatinib, who have a& G! ~( f9 p5 `" z
durable complete molecular response might remain in CMR after stopping; ]) X5 Z2 w. y
treatment. Previous reports of patients stopping treatment in complete molecular( e! u9 m$ p( k8 W: L
response have included only patients with a good response to imatinib. We
2 g, y6 D2 e4 Gdescribe three patients with stable complete molecular response on dasatinib" q3 e7 u5 G' a- q5 _
treatment following imatinib failure. Two of the three patients remain in
8 Y, S9 j+ M3 ?+ \( w$ {complete molecular response more than 12 months after stopping dasatinib. In
4 D# s+ B' ^1 ~6 c. ethese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to9 F7 z7 n8 l% O0 u" \8 I
show that the leukemic clone remains detectable, as we have previously shown in, D! h4 S: n' Z. w( U; ~: `; C7 O$ Z8 F
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
' D: {+ @/ ?$ k0 ]$ Z* ~8 Fthe emergence of clonal T cell populations, were observed both in one patient0 y+ P/ L# K8 |
who relapsed and in one patient in remission. Our results suggest that the
2 g# F3 q9 X( ?characteristics of complete molecular response on dasatinib treatment may be* [" j$ {" h7 B1 a# Y6 v- e6 ]
similar to that achieved with imatinib, at least in patients with adverse
6 r$ c2 C+ X- r: g! B0 Q" vdisease features.
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