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。
% J" O" p8 J4 L G. j i 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 p h1 s, D
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作者：来自澳大利亚5 R5 \! a2 _% X( b
来源：Haematologica. 2011.8.9.
& g" d& j5 N; k, s5 E- D# `2 aDear Group,( R+ u0 _0 m; q }7 H
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 i7 c7 E% R2 H, g! F+ o
therapies. Here is a report from Australia on 3 patients who went off Sprycel' c" D6 R6 y1 Y
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
: X; n0 z) z% p' ]7 fremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel) ^- u" H& K0 ?. r% }
does spike up the immune system so I hope more reports come out on this issue.0 F% u; o! t4 S$ |. [/ N) W
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The remarkable news about Sprycel cessation is that all 3 patients had failed! w3 j& [: q* j
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
! A8 t- l4 k( ?; ?different from the stopping Gleevec trial in France which only targets patients
% y2 K% c6 n" p; y3 j0 Rwho have done well on Gleevec.
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- U* l/ m# M& {( K4 K4 m: W4 [$ _7 _Hopefully, the doctors will report on a larger study and long-term to see if the2 c' q9 K& _9 L7 k5 a( e
response off Sprycel is sustained.
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Best Wishes,& Y2 |, C6 u0 j, k
Anjana0 D( [" v Q- f" K
2 a6 {( F1 J R# x
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Haematologica. 2011 Aug 9. [Epub ahead of print]- ~9 Q D# l4 x: t/ u4 S) `
Durable complete molecular remission of chronic myeloid leukemia following2 v2 c- n; I, _- m1 C
dasatinib cessation, despite adverse disease features./ w6 @- q' S& \$ d6 b# z
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
" p4 u- N" E f7 zSource; i l5 S# W+ h/ j9 S/ d% J, w
Adelaide, Australia;! f6 ~: P6 o& P1 {0 p
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Abstract
4 O; Z5 I7 d( \. b/ H2 rPatients with chronic myeloid leukemia, treated with imatinib, who have a' j$ L8 W% ^( E$ g& A0 D/ ?
durable complete molecular response might remain in CMR after stopping
8 P* ?; z! W& j& p% a# q1 V- |treatment. Previous reports of patients stopping treatment in complete molecular
( @0 c1 F# w! fresponse have included only patients with a good response to imatinib. We
3 k; h* }$ V+ ]describe three patients with stable complete molecular response on dasatinib
0 S3 T4 J1 `$ |/ \" U3 Qtreatment following imatinib failure. Two of the three patients remain in* ?% S$ `' T* z0 g* z9 _
complete molecular response more than 12 months after stopping dasatinib. In5 W8 n# `& u5 ^5 @3 |& G
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to# j) `. n! b, @& P+ y( x- Y" W& A+ P' P
show that the leukemic clone remains detectable, as we have previously shown in
4 J+ K* d4 k* I8 r* z( u( pimatinib-treated patients. Dasatinib-associated immunological phenomena, such as) H/ [0 S, H! ?0 g
the emergence of clonal T cell populations, were observed both in one patient
/ L1 \; G' B; e, nwho relapsed and in one patient in remission. Our results suggest that the
d# C$ S r, Y; n) bcharacteristics of complete molecular response on dasatinib treatment may be
! P! p4 f8 n! e \" r2 dsimilar to that achieved with imatinib, at least in patients with adverse
: T! y# q% C8 ?$ w) ?! {* gdisease features.: y& y' |4 s& E( o5 ^9 G
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