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。" l9 I: {* _* A# A1 y2 q
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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0 a* d0 g, v2 ^- U' F8 ^作者：来自澳大利亚* S5 }0 F$ U5 b7 Q7 W0 ?
来源：Haematologica. 2011.8.9.) A, J+ t7 K2 B3 V7 T
Dear Group,# U6 w/ F2 b! ?, }$ W6 K3 G
/ @+ g. w5 ~0 W( r9 OSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 E K' C) S+ y, btherapies. Here is a report from Australia on 3 patients who went off Sprycel
; q1 V, i% ]4 Fafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
! B0 X3 Q B# h( t9 @remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- W7 c5 q! x/ A1 H Bdoes spike up the immune system so I hope more reports come out on this issue.# |' d/ S1 c' d+ _/ M
5 O+ n9 t' P* b' g& s; ?/ @6 TThe remarkable news about Sprycel cessation is that all 3 patients had failed( [( U7 p9 }: H0 b+ l% \' X; s% Z
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
0 I$ B% [4 [1 I& x/ Q! x! Z8 pdifferent from the stopping Gleevec trial in France which only targets patients# j8 s- s7 a' z/ d7 c7 D% R
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
; \2 `0 Y# j* H6 E% I, Q& ?; T$ nresponse off Sprycel is sustained.' k; y2 R- L9 a" G, S: e! e
# l A* T) n" T# X% ~0 @5 Q4 P
Best Wishes,2 \. n. w! w2 g+ S4 I
Anjana! o4 M7 J1 s+ l$ F7 ]# ^" A2 [
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Haematologica. 2011 Aug 9. [Epub ahead of print]4 K3 o2 z2 h8 h$ Y
Durable complete molecular remission of chronic myeloid leukemia following: W& ?% Z+ J7 b& }
dasatinib cessation, despite adverse disease features., C3 U( B5 S' B3 ? C8 n: ]
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
* [( [) p! L: x* r7 {# ~Source0 V$ T3 _! D' e" X4 g! `1 Y
Adelaide, Australia;
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, O! Q7 O& V5 GAbstract
1 ]+ e; y+ ^& Z- O2 a& @$ uPatients with chronic myeloid leukemia, treated with imatinib, who have a
1 i; h% t( o1 B. hdurable complete molecular response might remain in CMR after stopping
* ^8 Z3 q+ }) L" d+ Ytreatment. Previous reports of patients stopping treatment in complete molecular. S/ N& Y. R2 }) f
response have included only patients with a good response to imatinib. We
1 K+ Y# U: y% J* @describe three patients with stable complete molecular response on dasatinib9 O8 b9 A' T, l3 H. N/ Q; ^ F% K
treatment following imatinib failure. Two of the three patients remain in
8 A6 O, B1 U' M/ y- e: u* dcomplete molecular response more than 12 months after stopping dasatinib. In
! S/ ^3 d7 W4 M% t- W5 _ Xthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to# ?, k) \* j" l, w) A4 p
show that the leukemic clone remains detectable, as we have previously shown in
& X! ]4 Y5 d3 ?' Y5 aimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
5 o& Y" {* ]' y% z3 ^+ ?* u. B' P+ ithe emergence of clonal T cell populations, were observed both in one patient% O) q) |8 k! t% v/ o1 N
who relapsed and in one patient in remission. Our results suggest that the
! }* ~6 H% O6 F) |& N: Lcharacteristics of complete molecular response on dasatinib treatment may be: o5 r% F+ A/ y
similar to that achieved with imatinib, at least in patients with adverse' f7 |6 Q; R. d% \( z* y7 o% h
disease features.
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