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。3 l( d* Y) s$ I O9 ~
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。3 s+ c& ^+ R3 u' A' k
- ~4 X% J ?4 O* m8 j作者：来自澳大利亚
! t) x# _8 |% x. r7 s- p来源：Haematologica. 2011.8.9.5 p- P2 |1 M. m
Dear Group,
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3 _* Z: V$ b1 q; }9 z* USome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
' A! |+ D3 _' I" c; R; z9 wtherapies. Here is a report from Australia on 3 patients who went off Sprycel a5 O: i3 _9 @. a/ v0 X
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients {3 x& }- t; C6 e0 Z2 E
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 e8 Q/ _0 D& X) `3 F4 I+ S. o H k
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 failed3 z$ f( R# ^, D2 x
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
) x+ }) l8 T, Bdifferent from the stopping Gleevec trial in France which only targets patients( ?" T* b2 Y" G2 k* w M& r1 \* F
who have done well on Gleevec.& X& r- B& T6 Q ^6 y" @7 i
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Hopefully, the doctors will report on a larger study and long-term to see if the0 V f, m0 f( g! Q) d
response off Sprycel is sustained.1 T. M0 T; X0 S& ]: @; I* |& C) p
1 a* p( q1 ? q
Best Wishes,4 [7 D% f6 U$ `, t* _ F
Anjana; P0 A! s9 t: [; x3 z4 \) e
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3 ?" ^9 A0 n& t# Z/ ]& [7 U4 ?$ A# [/ ^4 P* Q3 d
Haematologica. 2011 Aug 9. [Epub ahead of print]- S! Y- ~: q# V8 Q2 P% Y
Durable complete molecular remission of chronic myeloid leukemia following1 A# N6 X! t3 k) }' \6 c# Z
dasatinib cessation, despite adverse disease features.) L' ]0 a) N0 u& k
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( p* k. K% C0 y$ b& K) p
Source
. ?3 E c0 Z$ x2 |; @Adelaide, Australia;
4 L+ ^: ^* D+ f. F5 q! B) P( V3 B
8 Y9 p2 Q) h; E+ v; x, c* FAbstract
8 j7 f- s$ i- b1 i& ?; tPatients with chronic myeloid leukemia, treated with imatinib, who have a/ g. ?5 r9 v+ v$ ?; ~& x0 d1 M$ Q) P! e
durable complete molecular response might remain in CMR after stopping/ M& X1 t( b& r4 p5 l$ v
treatment. Previous reports of patients stopping treatment in complete molecular
8 U4 l5 `8 q3 }! O; nresponse have included only patients with a good response to imatinib. We. ]5 g/ K+ V& }0 H
describe three patients with stable complete molecular response on dasatinib
/ i- J0 F G' C/ _0 btreatment following imatinib failure. Two of the three patients remain in/ d! c/ x- e; P4 n7 |. z
complete molecular response more than 12 months after stopping dasatinib. In
( T5 Y( } n2 K' Z# N+ c# ]these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
3 X( n/ `3 @2 r! O7 L! yshow that the leukemic clone remains detectable, as we have previously shown in# V7 z! H% [8 g- C4 E$ ]
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
. r" C a, A+ Y% U0 Z1 \the emergence of clonal T cell populations, were observed both in one patient
5 U! R1 v# {. V% Uwho relapsed and in one patient in remission. Our results suggest that the
; G$ Z5 x* w8 D! Xcharacteristics of complete molecular response on dasatinib treatment may be
5 S+ K- X- j# r$ T* S' H3 lsimilar to that achieved with imatinib, at least in patients with adverse
2 K$ J( X8 a" Kdisease features.
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