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。: c2 y0 {; i6 I) w
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。* E0 r9 y: |" f# Z: P
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作者：来自澳大利亚
. I4 g5 ~4 v: {9 ?* u( F7 {来源：Haematologica. 2011.8.9.
& N; V2 {: t# W8 Z9 a9 g, X9 [/ sDear Group,' ]0 R* U/ c6 h$ k$ F
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML0 K, Q& A" q8 b& B# f
therapies. Here is a report from Australia on 3 patients who went off Sprycel
) f$ R/ [, \; K- [: x. Y: `2 T; yafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients; C4 N$ K3 H) [1 d" ]
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
( n {, }& V9 I6 \. O0 Tdoes 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 failed
) G; u7 @+ p. C8 TGleevec and Sprycel was their second TKI so they had resistant disease. This is/ `( C4 w9 l! m1 J K2 h
different from the stopping Gleevec trial in France which only targets patients$ ~ b: `% q# e: ?4 J
who have done well on Gleevec.8 V1 l" g7 r1 E3 t7 j/ S
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Hopefully, the doctors will report on a larger study and long-term to see if the. W1 A1 a8 p! K
response off Sprycel is sustained.- e7 p: L0 d( W% ~; M9 C
4 k: x6 X7 p$ q& \5 JBest Wishes,
6 r, v; g. i1 ^4 F0 e9 a7 ^Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]% T! y+ N2 K! D1 w1 x
Durable complete molecular remission of chronic myeloid leukemia following8 f- n% V& n: ]3 B" H
dasatinib cessation, despite adverse disease features.) E! p9 ]' i3 X
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
6 E3 M! z' F( I hSource" Z1 c" [& m) f( X' s" r: u9 Q
Adelaide, Australia;; V( A' H3 |" R2 n) W Q
/ n U9 g9 y: b3 h3 Y& DAbstract
/ h8 F; T* R8 ~. w' wPatients with chronic myeloid leukemia, treated with imatinib, who have a
/ m2 a, K A& q& r$ t0 N7 ndurable complete molecular response might remain in CMR after stopping F2 S3 E$ u4 t! p: p" Z
treatment. Previous reports of patients stopping treatment in complete molecular
5 }3 ]- n( v% ^3 x4 j6 qresponse have included only patients with a good response to imatinib. We
" [/ i' w% @. [. ~4 g tdescribe three patients with stable complete molecular response on dasatinib V) U- G. c1 G$ u1 \+ n
treatment following imatinib failure. Two of the three patients remain in
; C5 Z8 {" h% v8 p, }complete molecular response more than 12 months after stopping dasatinib. In
0 ~% P1 {! L# x6 O+ t% nthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
+ D* j) B3 B- s9 l0 j9 O/ E' Rshow that the leukemic clone remains detectable, as we have previously shown in
, [/ i; t: |' H4 G' d& D4 oimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
2 O" P* D& P8 r Jthe emergence of clonal T cell populations, were observed both in one patient+ |6 d" o( I3 q$ x. f
who relapsed and in one patient in remission. Our results suggest that the
/ l* g2 Z& ]0 ^9 F. B* J2 K8 qcharacteristics of complete molecular response on dasatinib treatment may be: ~- a- T" ]; ~+ `" i6 r4 {
similar to that achieved with imatinib, at least in patients with adverse
$ ^/ h. ^+ J: j( u( edisease features.
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