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。
& Q# H+ v# m3 w2 C' t 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: J% t* w4 \. @6 e
来源:Haematologica. 2011.8.9.1 W: F; }* z5 ~+ X
Dear Group,# ?, b$ ^! n# w4 R, c( L
" [- \& T* l+ T( C: w7 NSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
2 C0 k! B. v8 V% Ytherapies. Here is a report from Australia on 3 patients who went off Sprycel) t- S5 G( A+ i, d; D. A
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
; X9 |2 y5 U4 Y1 O' _+ a- m# F/ @remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
' i9 w& Y( y6 ?7 u: {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
) k+ I; L# d, b; N# Y+ }; XGleevec and Sprycel was their second TKI so they had resistant disease. This is" U w: [* U* i$ J, X
different from the stopping Gleevec trial in France which only targets patients& s5 F8 q/ {( y' A8 q
who have done well on Gleevec.# _, J9 [+ ]; C) A
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Hopefully, the doctors will report on a larger study and long-term to see if the6 Q$ A! j% Y4 E4 n
response off Sprycel is sustained.
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+ R' A: u$ _& c- Q6 g, I' }$ xBest Wishes,
1 t" z9 e3 T' l3 B% I7 `Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]3 d+ O8 c' N/ r+ Z
Durable complete molecular remission of chronic myeloid leukemia following, N7 z2 f `! c% D
dasatinib cessation, despite adverse disease features. N9 h$ Q' F/ Q% q {: o7 n: ?
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.$ O# j3 h8 r+ |
Source% ^4 D- I6 K' c# k. ~" o9 }
Adelaide, Australia;$ E( Q) V& m+ @
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Abstract
4 O* @$ p. d& l) X2 E. YPatients with chronic myeloid leukemia, treated with imatinib, who have a
; B7 \! M7 A% cdurable complete molecular response might remain in CMR after stopping& C/ p) K4 ], c% V0 }) i
treatment. Previous reports of patients stopping treatment in complete molecular
6 K. x8 ^ C' O" O" Iresponse have included only patients with a good response to imatinib. We5 O! P0 l: |) C8 O1 B( ]; s, w
describe three patients with stable complete molecular response on dasatinib% O1 O5 g, S+ V& \1 f; I' |
treatment following imatinib failure. Two of the three patients remain in& A5 r5 B1 t$ w
complete molecular response more than 12 months after stopping dasatinib. In
/ p1 @9 }( `, x Z# j, Ethese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' [) U3 T" D( A- C; Bshow that the leukemic clone remains detectable, as we have previously shown in/ Q( @) k3 f1 U( x# J: a, }" C+ l1 v
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
0 F0 J+ G$ M4 u( Vthe emergence of clonal T cell populations, were observed both in one patient3 b6 p3 [* X! P& U$ M" |9 O
who relapsed and in one patient in remission. Our results suggest that the, P2 `& m4 H9 w0 b' D
characteristics of complete molecular response on dasatinib treatment may be, s; C0 x M/ _$ z1 H4 Z z
similar to that achieved with imatinib, at least in patients with adverse
7 x5 Z+ N6 L" }disease features." r/ ?! R2 n: P G
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