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 ^. O' D4 b- D9 V6 c1 i
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。9 u) `& c9 h' J& H1 H$ f
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作者:来自澳大利亚
* G/ V+ ~' d6 }+ \' K来源:Haematologica. 2011.8.9.
/ Q) _0 t9 _2 o1 F! `9 Z+ DDear Group,
, ~; ?& h4 {+ X) W1 @* s" ~' V* D+ E7 ?9 X0 x8 |+ X( h
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ y+ y7 @* L/ r8 i
therapies. Here is a report from Australia on 3 patients who went off Sprycel' Z9 u( t: [6 a6 v( q5 ]
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients4 @" y& }+ Y& D# A
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel8 g" C, r7 `2 h4 R! ?( F, o
does spike up the immune system so I hope more reports come out on this issue./ ^& P* k- _8 D2 j5 O+ q
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The remarkable news about Sprycel cessation is that all 3 patients had failed
* T" S2 M4 w2 f! X- F" m1 z. ? kGleevec and Sprycel was their second TKI so they had resistant disease. This is
* {- a) s. K% L: _, x5 qdifferent from the stopping Gleevec trial in France which only targets patients
$ Z7 p) P1 i2 f5 L( P6 zwho have done well on Gleevec.3 O( L( R9 a& a$ o7 O4 ]0 q/ b: \ s$ E
9 v& f3 @. g* ]
Hopefully, the doctors will report on a larger study and long-term to see if the
! Z% i3 P* ^# I* lresponse off Sprycel is sustained.# \6 ?2 [$ ?( d% ~" h
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Best Wishes, G7 i* M% H J+ v( G5 S
Anjana% @6 D, e4 c8 b% _& q- [
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$ J+ \; f. g8 ?8 xHaematologica. 2011 Aug 9. [Epub ahead of print]
4 Q$ x4 s6 W1 d3 { ~8 \! W6 HDurable complete molecular remission of chronic myeloid leukemia following0 C& l! C! w; ~ M
dasatinib cessation, despite adverse disease features.
) W g# J- ~% e( Y( J: O5 P8 {# gRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.7 t5 d. {" ?5 W9 W! f2 o
Source
% P" ~% E- F+ EAdelaide, Australia;' y0 f5 I' o8 |1 Q7 ~
+ q7 P, ]9 P. j+ }8 y0 R
Abstract+ r4 P7 l. I9 @/ `0 D5 `& C
Patients with chronic myeloid leukemia, treated with imatinib, who have a
y" g. i& c) z5 B! X& }: ^durable complete molecular response might remain in CMR after stopping
9 U! w& U3 b$ m; j5 @7 |treatment. Previous reports of patients stopping treatment in complete molecular
3 T" k) S7 D$ W6 K% Q* @5 r6 xresponse have included only patients with a good response to imatinib. We A i, a# h x% \) H
describe three patients with stable complete molecular response on dasatinib' }5 j4 w3 r! _3 [3 k0 ^# y
treatment following imatinib failure. Two of the three patients remain in
# Q: V$ y# g; e4 g3 ecomplete molecular response more than 12 months after stopping dasatinib. In
9 t1 f6 i% E: Q4 k) l0 N8 b7 j9 sthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to7 V$ ~+ ~9 u f0 U3 Z" z3 [
show that the leukemic clone remains detectable, as we have previously shown in
8 x6 ^. V' N" Q5 e+ f) n+ ]6 D' Bimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
; a' v% ~; U7 b$ v. `5 U' ithe emergence of clonal T cell populations, were observed both in one patient, n# R) m8 ]0 f& R5 h N- V
who relapsed and in one patient in remission. Our results suggest that the
8 u! T9 V0 t4 Y, p- |- q! v( G2 Pcharacteristics of complete molecular response on dasatinib treatment may be
( t0 I9 j& g/ W- l/ bsimilar to that achieved with imatinib, at least in patients with adverse% W5 y/ H2 T0 D# L! o5 s
disease features.+ K& k- `( `' K4 ]$ a& z$ r$ {* I
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