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。& g0 j9 K& _& Q" Z& ?" K, f
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. s$ s) T6 q) S' b2 O! d8 \% o
. X2 t& {8 f/ m作者:来自澳大利亚
% a/ e. \! U$ C I来源:Haematologica. 2011.8.9.% `( A" C/ H; Z* C( t8 ]
Dear Group," [% O2 S6 J; U p8 g9 o$ k9 M* [
& U) Y4 K8 r/ t; X& \* u) V8 \Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML* x8 ^/ v2 Z' J6 ]( T4 o; @
therapies. Here is a report from Australia on 3 patients who went off Sprycel5 t+ d" Y2 p) L# `" c
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients: g" l5 m/ w8 G& b5 x# A# u
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
, r2 H% X8 d% M& X$ h5 n+ g( Gdoes spike up the immune system so I hope more reports come out on this issue.* F# Z) \* \& _
' m1 j6 W/ ]! ?- F, u
The remarkable news about Sprycel cessation is that all 3 patients had failed2 U: x# c6 Z' f0 {
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
" x$ I A8 f" r9 G% e3 wdifferent from the stopping Gleevec trial in France which only targets patients( ~2 b2 N+ E( E; I) n& f6 N
who have done well on Gleevec.
: L/ G/ l. J+ b6 Y+ {) q& H$ L8 L) g8 k+ \1 B
Hopefully, the doctors will report on a larger study and long-term to see if the# O, J2 e3 H) Q; i% H/ w! }2 B# W1 R
response off Sprycel is sustained.) V: r& o# S( O0 [: S6 G
% ?, X: v% w- c) \
Best Wishes,
1 D/ `) M! Q6 |# NAnjana
, }6 G6 _' L+ c9 Y: R3 n0 {! d7 c6 G3 e9 @* q$ I1 f$ w
6 p7 }7 }: y* w8 B) h
& N8 Q6 m6 \9 w1 G7 ]Haematologica. 2011 Aug 9. [Epub ahead of print]- G! K7 c. d* A) y4 ^+ ]
Durable complete molecular remission of chronic myeloid leukemia following
' P4 g5 p$ x' t/ t) ydasatinib cessation, despite adverse disease features.5 f3 m/ Y/ w3 M1 v
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.4 c2 x( |, Q. X
Source
+ _3 {' `4 M& F& u9 V% EAdelaide, Australia;' b# i1 P+ S2 u; i- |, k) |0 }) l; W) H
7 Q3 [6 R( p1 E
Abstract4 A% a. c* B: v
Patients with chronic myeloid leukemia, treated with imatinib, who have a: P b' l5 X) K, s$ ~# f
durable complete molecular response might remain in CMR after stopping
% l# ?7 M7 j- C# streatment. Previous reports of patients stopping treatment in complete molecular
! ?, m. Q. |( d; z2 f/ gresponse have included only patients with a good response to imatinib. We
* g! l6 U. ~! v% e; W H1 U: H8 [+ Cdescribe three patients with stable complete molecular response on dasatinib# q& b5 S% o' m1 _
treatment following imatinib failure. Two of the three patients remain in ~0 G8 h% p* e4 c. o$ W
complete molecular response more than 12 months after stopping dasatinib. In
% R( o. e" J# h, a2 v# \6 hthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
# U& p* F7 k! f" oshow that the leukemic clone remains detectable, as we have previously shown in
- h5 P7 J, s% Y6 z3 g+ B- q2 zimatinib-treated patients. Dasatinib-associated immunological phenomena, such as. Z9 b# E* x( u0 y% |0 ~, I1 n' ^
the emergence of clonal T cell populations, were observed both in one patient1 M& P% Q! u+ E6 c
who relapsed and in one patient in remission. Our results suggest that the' H! {0 l: T5 Z4 a! p; S
characteristics of complete molecular response on dasatinib treatment may be) I$ ^* ]3 P% ]/ y
similar to that achieved with imatinib, at least in patients with adverse4 k8 X7 J# L8 y+ ~
disease features.
5 j o+ N6 Y( Y) @7 ] |