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。5 U" h8 e* n' B, q: w" F
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。7 p) T( C1 }! Z0 B
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作者：来自澳大利亚, D/ G. [ v3 N- ~
来源：Haematologica. 2011.8.9.9 s c3 D' P2 q: y! i6 R
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML# v) Q; B& A/ c6 b6 c
therapies. Here is a report from Australia on 3 patients who went off Sprycel
' Y0 G5 |" G+ A0 e0 E) ]- Kafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
. `4 F# y; R5 Aremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
5 Y: u; i+ n- jdoes spike up the immune system so I hope more reports come out on this issue.8 ?% R- ~! F( a6 N& z7 {
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The remarkable news about Sprycel cessation is that all 3 patients had failed( `$ s1 R) r' u
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 n$ ^9 Y" F% e( S
different from the stopping Gleevec trial in France which only targets patients
+ `6 N( V( K. H" K2 _* awho 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/ t+ O+ b0 r/ U) v+ C8 h ?
response off Sprycel is sustained.
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8 A: k( F, G8 E7 g7 `Best Wishes,
+ z! i' H) t: z5 K4 I/ @Anjana
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+ R- z8 i6 x3 G* fHaematologica. 2011 Aug 9. [Epub ahead of print]
! z3 c' r+ y3 |( O# g, JDurable complete molecular remission of chronic myeloid leukemia following
- x3 \& D4 r R( i zdasatinib cessation, despite adverse disease features.
1 A, e" ~9 \' U& _# IRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
$ }- l6 [/ ^( `% a0 ?3 _+ D2 USource
* t( y9 J& ]* t4 y: rAdelaide, Australia;
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Abstract( t, W2 g/ \* R
Patients with chronic myeloid leukemia, treated with imatinib, who have a9 K0 p e0 ]2 M/ ~6 H* q* q# l7 b
durable complete molecular response might remain in CMR after stopping/ @; J4 J7 J* e6 n# q d# T& d
treatment. Previous reports of patients stopping treatment in complete molecular
3 I& F& q0 M, N1 c w& lresponse have included only patients with a good response to imatinib. We' j4 g) x8 Y" Q2 {) X; S! c* k
describe three patients with stable complete molecular response on dasatinib
7 e1 ]( Z/ _# i; m/ Mtreatment following imatinib failure. Two of the three patients remain in# ]% n; X8 S5 v5 i+ T% [3 z! R, P9 X
complete molecular response more than 12 months after stopping dasatinib. In
( d- `" z3 t9 O6 J. r* Nthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 \% E0 d, s* s2 U) p& o
show that the leukemic clone remains detectable, as we have previously shown in
: w) x) Z; c- kimatinib-treated patients. Dasatinib-associated immunological phenomena, such as+ k5 s; g1 D' V6 m7 {/ [5 R4 G
the emergence of clonal T cell populations, were observed both in one patient
8 b S6 p6 r& S/ Q' i G% `who relapsed and in one patient in remission. Our results suggest that the
+ H- j3 k# u$ y- n* icharacteristics of complete molecular response on dasatinib treatment may be! O* ~8 j; k* K( t/ O
similar to that achieved with imatinib, at least in patients with adverse
2 R' F! a! c1 \6 ^disease features." W0 }: I O0 v; F4 l
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