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 A; N) k0 \3 F+ ?9 _
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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) r0 Q/ d7 N0 C. ?作者:来自澳大利亚4 V3 }" `" Q& l4 H( W
来源:Haematologica. 2011.8.9.7 j! j4 |7 @3 Z4 Z& z. ~4 N+ @
Dear Group,
0 }# i/ j* b$ Z7 [
) c: d d! @ c* R, ]4 \3 kSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
% E" N: G# M2 n( i- ytherapies. Here is a report from Australia on 3 patients who went off Sprycel: H/ w* }! a3 E Y0 U% w
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ u+ q) @: |5 h9 bremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
9 i* l9 |0 d+ ~does spike up the immune system so I hope more reports come out on this issue.5 W" X! ]+ d) S0 ]9 a5 E+ O1 e
6 m# }9 v1 N& q0 vThe remarkable news about Sprycel cessation is that all 3 patients had failed7 [% u, J7 n) [8 M# b# d
Gleevec and Sprycel was their second TKI so they had resistant disease. This is3 n2 F0 C+ B4 o% o' n
different from the stopping Gleevec trial in France which only targets patients. B6 N# V& V4 n4 ?" W# V0 j* ^' A6 W5 P5 U
who have done well on Gleevec.: s, w8 m6 Q+ p1 |1 j6 V' J# D- L
6 I( n" T+ j2 w; c1 O. KHopefully, the doctors will report on a larger study and long-term to see if the
0 l3 W3 J2 j' \0 Tresponse off Sprycel is sustained.- N0 J: K% N( b! k, e2 f
8 g% z* x. y, ?( [6 m, \
Best Wishes,
6 U' u1 E# i1 w1 v6 c8 }7 g$ [. ]0 IAnjana7 |" g; O- g3 q' m! `* @
$ b: x! w' m U( N; Y
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Haematologica. 2011 Aug 9. [Epub ahead of print]
f/ h" S& P) v5 ?Durable complete molecular remission of chronic myeloid leukemia following& k/ Z- d; b. o" Z9 F
dasatinib cessation, despite adverse disease features.$ e: _# T" Q5 B. \. Q) J( h# d
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
6 S1 _( @9 P8 T; @8 B4 I( uSource( v0 E3 }; e; P0 g9 N" _
Adelaide, Australia;
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! i; P+ d; c+ D5 a; a/ ]Abstract
3 Z) X5 I; q) e0 X0 _Patients with chronic myeloid leukemia, treated with imatinib, who have a
( d+ Y2 }# ^7 a( Q3 l2 H* jdurable complete molecular response might remain in CMR after stopping
) t" `4 K: q% B) n1 y: [- ^treatment. Previous reports of patients stopping treatment in complete molecular
+ o8 ]0 Y$ O3 ]0 Y! wresponse have included only patients with a good response to imatinib. We
3 e; }6 t5 H( |; f, wdescribe three patients with stable complete molecular response on dasatinib7 }1 D. @; _4 U
treatment following imatinib failure. Two of the three patients remain in
Y) }. d9 k9 G0 i4 s* jcomplete molecular response more than 12 months after stopping dasatinib. In
; x! j, [1 s/ V+ \! D; sthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
" C& m# g- c& l. N/ U' dshow that the leukemic clone remains detectable, as we have previously shown in" [1 R" h( x- v6 | D& ]. w8 Z* d" q
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ S5 V$ i+ [/ n# t5 i& y& Athe emergence of clonal T cell populations, were observed both in one patient, {# \6 D$ B+ I, g' Q
who relapsed and in one patient in remission. Our results suggest that the I2 P w9 h. Y; i3 D2 `) y
characteristics of complete molecular response on dasatinib treatment may be
6 ~* p$ f; p% P9 Q( Bsimilar to that achieved with imatinib, at least in patients with adverse* P1 Q8 F% j5 Q& c; E: L9 Y+ }: h7 ^
disease features.0 g- g4 h; ^4 E. `+ u* ]/ D1 W
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