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。) m: W! o* L2 M, @+ 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。, ]$ `$ T: ^. x# `* W0 `
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作者:来自澳大利亚2 S% w- E) x9 D# D2 q5 O
来源:Haematologica. 2011.8.9.
6 w8 V) {5 w; Z7 h) t; ?Dear Group,, T( m7 C- j; y3 I2 V! | X5 l- b
$ x. `- U& f2 w, T! I1 K8 DSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML' \3 n, P7 E7 @# T Z" p: ^
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 r. c4 K4 A! g, Y
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients, a ?) p& s3 r. y$ d# ^
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
, v, A# d+ \1 N5 rdoes spike up the immune system so I hope more reports come out on this issue.* ?" B% j1 \3 p5 Z- d
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The remarkable news about Sprycel cessation is that all 3 patients had failed
- k6 |. n5 h5 h: tGleevec and Sprycel was their second TKI so they had resistant disease. This is3 ]; g R9 \ h$ d7 p" s$ ] {
different from the stopping Gleevec trial in France which only targets patients9 ]3 c B4 H5 ^: K' [
who have done well on Gleevec.7 A9 t2 i& `/ }8 i1 t1 M \+ L) B
1 n2 t! ~( ~- O6 h$ P0 D) g8 \Hopefully, the doctors will report on a larger study and long-term to see if the
8 `0 d5 `! d' Xresponse off Sprycel is sustained.
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2 H) f, |$ D; U. r( k' O0 s' L3 U$ {& OBest Wishes,
* c, p9 I3 ~6 q% }9 ?+ {7 aAnjana
9 Q2 o7 A" K7 `$ L7 c8 \2 `, \& ]9 Z. u* m
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Haematologica. 2011 Aug 9. [Epub ahead of print]+ N+ E3 I p; [& q- ~, v7 ~$ [
Durable complete molecular remission of chronic myeloid leukemia following. R- r2 _+ q( f9 a; z3 u
dasatinib cessation, despite adverse disease features.
, }0 J1 {/ q) y" d2 Z# z2 x/ l y) hRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( f5 H- [$ O7 u% G' u
Source* @8 h7 d" p3 X& I* B& @
Adelaide, Australia;
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Abstract5 y& F5 g2 c9 @% X# r
Patients with chronic myeloid leukemia, treated with imatinib, who have a: Y1 o! y \# o2 ~* s
durable complete molecular response might remain in CMR after stopping) @, e% ^/ V, m0 S p, j
treatment. Previous reports of patients stopping treatment in complete molecular; U( J: K- l" V: C# c& l/ E( N$ E
response have included only patients with a good response to imatinib. We! S9 Y3 O0 Y2 K1 e3 \
describe three patients with stable complete molecular response on dasatinib
9 x4 A1 j {) [5 G% Z2 ^3 m' wtreatment following imatinib failure. Two of the three patients remain in
+ {6 w6 {7 j3 d ncomplete molecular response more than 12 months after stopping dasatinib. In
9 q2 u$ j, g- m+ A0 L0 Pthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
( I# r7 X- B4 i. X/ U4 Yshow that the leukemic clone remains detectable, as we have previously shown in
( r8 f j7 h j8 s2 J) W/ Aimatinib-treated patients. Dasatinib-associated immunological phenomena, such as0 H/ n6 b2 B* @' I
the emergence of clonal T cell populations, were observed both in one patient
2 q+ n% o. i+ pwho relapsed and in one patient in remission. Our results suggest that the+ Y7 K8 [1 C* W
characteristics of complete molecular response on dasatinib treatment may be- h/ x2 E. V& r" Y. V6 B8 y
similar to that achieved with imatinib, at least in patients with adverse3 f( i W; c9 C3 C0 }9 L& j
disease features.0 ?: r2 \# I! G, x' ~% _
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