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。
3 V! @) h5 V3 B 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。0 A4 z" s) O% P( L- a t; j) K
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作者:来自澳大利亚
8 F% E& N8 F7 E, m* n来源:Haematologica. 2011.8.9.# P, a: _0 _& |8 i! y
Dear Group,* w& _& m2 j$ L
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
& W, y3 _+ v0 G; c5 Mtherapies. Here is a report from Australia on 3 patients who went off Sprycel7 U! L. ?; N9 ]9 S
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients1 j; F: g4 V. }9 s5 j S
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel: R/ p+ b: k9 I/ n' Y
does spike up the immune system so I hope more reports come out on this issue.5 S) J3 G; _; M( O4 c8 N; X V( [
% ~8 T4 K8 d8 s* W) m0 ZThe remarkable news about Sprycel cessation is that all 3 patients had failed. A, [3 Y8 j+ v- }4 q1 Y
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
( c1 A8 j! P9 p# F5 ddifferent from the stopping Gleevec trial in France which only targets patients
5 ?* B* x4 k" \* x0 D' cwho 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
! n# H" b& i& w5 y( K, gresponse off Sprycel is sustained.5 x' ^) b* ?& E; p0 Q1 `# ^
[4 E( K5 v8 E8 F; e# kBest Wishes,
8 [- t5 J2 `8 A6 f. A. a. HAnjana6 \+ x1 u$ T6 Y- P. G# R
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Haematologica. 2011 Aug 9. [Epub ahead of print] x! `# k6 H6 @/ f
Durable complete molecular remission of chronic myeloid leukemia following
+ d4 A! N' ~6 j% c# `dasatinib cessation, despite adverse disease features.
0 d9 } N- P# }8 l% { ORoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.% y/ G0 Z( q7 b6 X9 ^/ X& v2 b; l
Source
& M% ?9 |) S" H0 ]$ W% S5 ~. w1 ^Adelaide, Australia;9 t! I6 L8 a, e# \) b
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Abstract2 [" i0 g$ I) Q' j6 {
Patients with chronic myeloid leukemia, treated with imatinib, who have a
8 ]9 Q3 L: i; p$ ldurable complete molecular response might remain in CMR after stopping
3 {7 x4 A8 T& B% g) i8 Btreatment. Previous reports of patients stopping treatment in complete molecular
' c$ p, [2 c* c3 W: Yresponse have included only patients with a good response to imatinib. We
/ M9 K8 e1 Z, Y8 `) vdescribe three patients with stable complete molecular response on dasatinib# R6 {7 Y8 g# ]" Z
treatment following imatinib failure. Two of the three patients remain in
2 H* |3 k5 b7 {' ~complete molecular response more than 12 months after stopping dasatinib. In0 s1 C' B# J9 h
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to' o6 E0 p, T y0 o# P
show that the leukemic clone remains detectable, as we have previously shown in- v, Q& N, i- g
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
$ f7 [* g, B2 m2 L4 L! C- ethe emergence of clonal T cell populations, were observed both in one patient
3 [( }% |% w+ c! H6 zwho relapsed and in one patient in remission. Our results suggest that the
: z3 x' ~4 y1 l" o: Gcharacteristics of complete molecular response on dasatinib treatment may be
7 F* [! d( u9 J) }# T4 K& a6 esimilar to that achieved with imatinib, at least in patients with adverse
( V5 r' G6 j" X9 Y$ z) Ydisease features.
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