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。
a m8 Q, V" u+ J 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。# {- m$ O' l2 f$ a: Z/ j; O5 ~) j- G
: w6 h! h# t2 ]) v" |; j1 H作者:来自澳大利亚: R3 H. G9 b3 v; i: I I
来源:Haematologica. 2011.8.9.1 @- N0 ]3 D. J5 |9 T# V/ r
Dear Group,8 J6 p$ M; e* d
8 p) W) c7 ~: i4 g% x7 Y$ z
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
+ e' p1 x& Q- S( ntherapies. Here is a report from Australia on 3 patients who went off Sprycel; Q8 F* }% P* `9 t
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
1 o, {- H) E' _' f& ~remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel; V$ b: V" v' g1 F- A1 `* Q9 P
does spike up the immune system so I hope more reports come out on this issue.6 I+ n8 d5 Z6 Q1 I9 h& X1 W
2 ?! q+ m: n$ r- }# |- X2 K5 lThe remarkable news about Sprycel cessation is that all 3 patients had failed
1 k% |) J$ f8 s4 }, X4 u3 F% A2 k _Gleevec and Sprycel was their second TKI so they had resistant disease. This is
a2 I3 Z$ h4 }! O7 ^' |6 Wdifferent from the stopping Gleevec trial in France which only targets patients" e' G1 r X, E$ D# T- z6 d
who have done well on Gleevec.
9 f% S" T( h. a" r
! X* `3 E3 j k) ]$ k1 ~Hopefully, the doctors will report on a larger study and long-term to see if the
. h+ N6 {4 P! T, P1 |' J+ dresponse off Sprycel is sustained.
% y- |9 {8 X+ K' H& ^
- z. a, q8 o; L& A0 b& P4 l& eBest Wishes,
, \4 U/ Z4 [3 `* nAnjana
l# a q( q4 l C
% X! S/ K$ A, m: i* w. ~' I- t7 W# w, w5 D
p4 ^* t) A7 c9 X* }9 K! I; u9 U5 E/ u
Haematologica. 2011 Aug 9. [Epub ahead of print]
: O+ a/ q4 N2 PDurable complete molecular remission of chronic myeloid leukemia following
0 l6 X4 w1 w: ^# ~% U* Hdasatinib cessation, despite adverse disease features.
* C" l9 x& o o( S: I& v7 w9 ~( sRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
9 D, \0 c' N$ I8 C1 USource
+ S+ a# ^1 i4 I6 a; P; X' [( g" GAdelaide, Australia;# @( M' G0 _* Y \: l
p6 ~% j" v" ~ d; \# M5 S5 g
Abstract
/ }5 G5 C- M: d- Z; M" PPatients with chronic myeloid leukemia, treated with imatinib, who have a
) c! f. O; ^+ c1 s7 ^durable complete molecular response might remain in CMR after stopping
" e% z7 A* g3 h' N- ?1 P$ J, t4 Ctreatment. Previous reports of patients stopping treatment in complete molecular
* B# U F# U( d0 lresponse have included only patients with a good response to imatinib. We
" a6 ?# u3 R4 @7 m6 [: ?describe three patients with stable complete molecular response on dasatinib$ z# ^; l8 d% i
treatment following imatinib failure. Two of the three patients remain in- o: R0 U& j; @6 q6 P& N& |- D6 c
complete molecular response more than 12 months after stopping dasatinib. In
8 B' ^' p2 u- cthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' J8 ]6 N' j" H+ n$ R( f5 Ishow that the leukemic clone remains detectable, as we have previously shown in
/ C3 P9 H) Y, K$ n& q! Dimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 J( V: X" V) kthe emergence of clonal T cell populations, were observed both in one patient/ s: r& o1 G3 F3 Q% G
who relapsed and in one patient in remission. Our results suggest that the s B, _2 M# v
characteristics of complete molecular response on dasatinib treatment may be( A3 Q: g# j2 y2 k
similar to that achieved with imatinib, at least in patients with adverse2 U9 ^1 g) W: }4 i [0 R
disease features.6 B. C+ |7 U! i+ P0 o
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