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。
$ x+ ]; F$ @' t% O u4 ` 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。- y5 B. C7 S. [1 \, p K. i) W
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作者：来自澳大利亚& E( [' f$ G/ \0 ?6 P
来源：Haematologica. 2011.8.9.
3 H" ?* s2 @8 z, _& P( tDear Group,
2 M3 C% T3 v5 E3 G& R8 }2 q. F4 q% o9 U4 R
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 C. K. `1 y. X: Y# o1 @ o
therapies. Here is a report from Australia on 3 patients who went off Sprycel
) s- K O( ]+ xafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients9 d _- N( D& @' a, J7 W" g. C
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
; I2 `5 ?6 [: d6 V2 t. o8 R; d. Tdoes spike up the immune system so I hope more reports come out on this issue.
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! U/ s+ M4 _% v3 P" qThe remarkable news about Sprycel cessation is that all 3 patients had failed
, X" x* }; C0 v: D& SGleevec and Sprycel was their second TKI so they had resistant disease. This is
7 w r, t$ U. Q! `& E1 L6 Edifferent from the stopping Gleevec trial in France which only targets patients
. E. r+ A) I9 L6 s% _4 Y( Pwho have done well on Gleevec.
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! c# F& P% {4 M) H) I/ P+ ]Hopefully, the doctors will report on a larger study and long-term to see if the
% @8 }& H8 o% Gresponse off Sprycel is sustained.
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; ?8 k A* ]' k. ?& u& Q7 k" vBest Wishes,
/ V- [/ h+ \: T4 cAnjana
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+ {. ]1 _: e j& t' {. KHaematologica. 2011 Aug 9. [Epub ahead of print]
+ ?; K( T3 D2 ^! K+ ADurable complete molecular remission of chronic myeloid leukemia following, z% f+ Y" I0 U- P) B
dasatinib cessation, despite adverse disease features." i. S" @& l0 ^* N3 }# _
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.) d4 o. |+ H+ m+ u9 @
Source
4 }! z1 z8 p3 Q( D5 W' z1 V" ]% oAdelaide, Australia;
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Abstract
2 Q/ j: [4 K( w; vPatients with chronic myeloid leukemia, treated with imatinib, who have a
7 [ M$ v3 j( Q% Bdurable complete molecular response might remain in CMR after stopping
? D, y% X8 f: I/ ]8 R& K4 ?treatment. Previous reports of patients stopping treatment in complete molecular
0 R& `. F) i7 V3 h6 @9 ]8 Zresponse have included only patients with a good response to imatinib. We" j1 k+ e0 @" e/ U
describe three patients with stable complete molecular response on dasatinib1 @8 d" R% C7 c
treatment following imatinib failure. Two of the three patients remain in
9 X0 e, m2 a, ^. a7 Ecomplete molecular response more than 12 months after stopping dasatinib. In/ N6 ?) t* w5 F
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
4 H2 |6 G j7 [ A0 C d( sshow that the leukemic clone remains detectable, as we have previously shown in
5 B8 q4 W; q: i% fimatinib-treated patients. Dasatinib-associated immunological phenomena, such as. N5 ?& o/ b8 Z7 G0 ?3 t+ e
the emergence of clonal T cell populations, were observed both in one patient( F, t! l) e* b5 A' f
who relapsed and in one patient in remission. Our results suggest that the
4 k1 F* M+ s6 m( s0 S; kcharacteristics of complete molecular response on dasatinib treatment may be
! b) H2 Y4 s. _; o4 q; esimilar to that achieved with imatinib, at least in patients with adverse4 ]" t0 K% M2 T+ s
disease features.
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