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。
8 s+ x8 f6 L" V* N+ ~$ q% 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。- u- \2 F6 U0 g* ~
2 x1 p. @" P* Z: a2 Y8 a作者:来自澳大利亚
; N; S9 A" _9 ]+ K. D; ?来源:Haematologica. 2011.8.9.
6 A' M |. [8 H. y1 r6 JDear Group,
" x7 o: {4 X7 \6 W6 e0 ^
$ a" e' Q& J* A" wSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, ?( v( K) k2 k; ^. k8 \6 F9 ?therapies. Here is a report from Australia on 3 patients who went off Sprycel
( g t7 `6 Z+ @: O$ J8 o5 \! c/ Dafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients6 j1 h9 M( T; S3 Y8 J& W
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel) |, V; R6 v; Z, n; [) I l
does spike up the immune system so I hope more reports come out on this issue.
/ w1 K# M2 f5 J# @6 z, ?% B7 T0 d, G- D8 d& d6 q% @8 p& t" P
The remarkable news about Sprycel cessation is that all 3 patients had failed5 b( v7 L/ F% H/ j3 c
Gleevec and Sprycel was their second TKI so they had resistant disease. This is- d' ]- f( H# L( X* r
different from the stopping Gleevec trial in France which only targets patients
6 q3 Z" |8 x, `0 O5 Awho have done well on Gleevec.' G: l* z/ r* h# o, _- o) K
) {5 D1 c$ K( U# D, GHopefully, the doctors will report on a larger study and long-term to see if the
7 A, M% R" c+ g; xresponse off Sprycel is sustained.
( C* G: ^) U3 i. w' e- u: u) m. i" |( e, m; |1 q1 O
Best Wishes,& a' _8 k. D( Z5 Q$ n
Anjana
9 p6 c# m& S0 h- h
# Q8 o& Y7 f2 f1 }/ N8 O0 |1 v- m7 h/ _2 s8 l. U' }! o: ?, P
! C6 x" d/ C; F8 o- P! WHaematologica. 2011 Aug 9. [Epub ahead of print]/ B( h! t! ~& ~- j8 s9 V4 D; s
Durable complete molecular remission of chronic myeloid leukemia following# {4 r$ x1 k! r: Y1 Q7 C+ q
dasatinib cessation, despite adverse disease features.9 ^! W0 {* @) i7 F' h& n; n
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP./ ~4 P/ E1 L. y) y
Source) a0 x" Q7 _2 S; c, Q# b
Adelaide, Australia;
" p3 @5 J4 m* F% U# R5 ?3 ~& k) B. N% Z+ Z5 |# z0 E5 m4 }8 t
Abstract9 @, ~* R$ N; w; ?, T
Patients with chronic myeloid leukemia, treated with imatinib, who have a& l4 r# F; q% y4 e, W9 a
durable complete molecular response might remain in CMR after stopping
* ~. U+ ^/ y/ o2 G0 H8 a* Streatment. Previous reports of patients stopping treatment in complete molecular) M& |* a* y9 a# r6 t
response have included only patients with a good response to imatinib. We) ~3 ]/ a) t9 I4 J
describe three patients with stable complete molecular response on dasatinib2 C& n- P" Y }# B$ X1 ?
treatment following imatinib failure. Two of the three patients remain in
/ @( a8 H5 ^/ y2 @5 _+ dcomplete molecular response more than 12 months after stopping dasatinib. In
3 p( t0 K3 s7 Q3 Vthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to% e1 r1 q9 }$ [: g6 x" D" Z
show that the leukemic clone remains detectable, as we have previously shown in
* ]# x4 n0 x5 X, Cimatinib-treated patients. Dasatinib-associated immunological phenomena, such as' h* z: d. W) z4 a! i
the emergence of clonal T cell populations, were observed both in one patient5 W6 ]" r& w7 L9 \- ]
who relapsed and in one patient in remission. Our results suggest that the& D2 M" |/ t$ H! {* R9 \+ p
characteristics of complete molecular response on dasatinib treatment may be# }$ c! f! w$ n+ l" \1 l
similar to that achieved with imatinib, at least in patients with adverse
/ e# {. h5 d! j pdisease features.; \$ _) H. v+ }; I! l4 e6 V z
|