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。
) H* J4 J" k- e 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。% b/ Y2 C0 ]) R8 p6 ^2 d4 s, _( o
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作者：来自澳大利亚" M* T8 `' r. t% S9 t
来源：Haematologica. 2011.8.9.
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# v& I6 H* G% @; v+ f/ L/ }Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML4 w: d2 j( M& I! T& g+ B5 Z
therapies. Here is a report from Australia on 3 patients who went off Sprycel
4 C" a+ i" K: n! z1 D% {after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, D' ] p! R0 i/ t Iremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. f) i2 {% a' S/ s. B0 b
does spike up the immune system so I hope more reports come out on this issue.( [- r3 F: d, W" f
) n! Z0 \5 d) GThe remarkable news about Sprycel cessation is that all 3 patients had failed# V- a; T& M+ b0 _3 W" f
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
$ n! m! P8 S# S: e [different from the stopping Gleevec trial in France which only targets patients
1 h8 u2 W, o5 Y. lwho have done well on Gleevec.
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0 r( h( X6 n2 XHopefully, the doctors will report on a larger study and long-term to see if the p9 ^/ @) E8 u3 o
response off Sprycel is sustained.
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; _. r$ C0 f3 M9 ]9 IBest Wishes,
8 f8 W) i+ p1 X+ G9 kAnjana
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T5 k8 v, O# T5 b+ ^' b! m% ^; g. M) L( S- t& m
Haematologica. 2011 Aug 9. [Epub ahead of print]
5 T2 `# R7 n" V- u5 P* O: o# o2 E* NDurable complete molecular remission of chronic myeloid leukemia following! J8 `$ `" P% K
dasatinib cessation, despite adverse disease features.6 q' G9 m# ~: S9 N
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
4 ]1 q1 ]: _: eSource
; X1 `( w1 I5 [: IAdelaide, Australia;
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4 i. |8 o! F0 B, J `6 `4 VAbstract
/ c( ~; h7 h' v) x$ m0 a% mPatients with chronic myeloid leukemia, treated with imatinib, who have a
/ ]4 }' s5 e: G% odurable complete molecular response might remain in CMR after stopping
9 A3 y% e6 J7 x8 ~+ G* \* Dtreatment. Previous reports of patients stopping treatment in complete molecular
8 A+ Y; j6 Z& j4 `) iresponse have included only patients with a good response to imatinib. We
7 D! X4 {. T9 J" P" v+ y) edescribe three patients with stable complete molecular response on dasatinib
9 F; l, i& @4 X# z/ b3 j! T' Btreatment following imatinib failure. Two of the three patients remain in* h& q1 R* j4 l2 Z# s: s$ h
complete molecular response more than 12 months after stopping dasatinib. In3 p" I+ L5 J1 U- ^3 {
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
" \$ R- |. K1 v% I" m6 m7 b2 ~show that the leukemic clone remains detectable, as we have previously shown in: C0 p) G+ R8 y5 U; o
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
' _- l7 Y8 d1 Q6 N% d5 ]the emergence of clonal T cell populations, were observed both in one patient
& Y7 S4 s6 U) G5 owho relapsed and in one patient in remission. Our results suggest that the
* O8 O) j7 j: n% q5 G! z0 pcharacteristics of complete molecular response on dasatinib treatment may be
0 e) K( i8 u2 N1 E: hsimilar to that achieved with imatinib, at least in patients with adverse
2 N, t; d# J& j% [1 D% fdisease features.
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