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。
, _) ~+ t. Q- {4 k3 N( w7 ?, [ 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 g; Q* x0 E* _3 G! r
- n5 H) i( R6 g5 {. o% H" d+ V* r! q
作者:来自澳大利亚
" C5 g5 K6 m0 B; F# s& ?6 u; T0 ^来源:Haematologica. 2011.8.9.7 ~8 }3 K3 T- r; ?! m
Dear Group,
9 f5 W7 M7 ~9 ]1 `9 k V% _5 X; z6 \. W1 r$ ]
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
& b1 c: ^! I+ P/ K' m! w0 ptherapies. Here is a report from Australia on 3 patients who went off Sprycel
4 b( o2 D) w1 S5 Vafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ a0 F# ?' X9 B8 J% |# t3 ~remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
; _! ~' z1 L9 R) `' u- jdoes spike up the immune system so I hope more reports come out on this issue.8 o$ L- \) a3 e* M' Y( P
$ R: b3 U4 t3 _+ S3 @/ g. B8 m0 YThe remarkable news about Sprycel cessation is that all 3 patients had failed0 U" f+ |3 V2 B4 Y- t- Z f4 E! W
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 x( |2 b/ f; ^
different from the stopping Gleevec trial in France which only targets patients
: E& j1 C5 }: t( s' \6 }/ ~. Ewho have done well on Gleevec.
, o0 ~4 }- Y) ?& [5 F8 k. P
& M. ^' z" y$ v' mHopefully, the doctors will report on a larger study and long-term to see if the
8 L# ]) `1 P/ ?. b' D) k' U' z$ jresponse off Sprycel is sustained.# P2 l8 C% v5 m: R1 X
3 R+ B$ u3 O" }* R# O1 ^Best Wishes,
( m! {/ E0 F; KAnjana2 G* ^7 X: c4 x l- S- T) B; ^
" k7 {! s7 f6 }& L
+ Z6 `6 x+ e3 U# Z0 R; n9 \' H; c) a9 J
Haematologica. 2011 Aug 9. [Epub ahead of print]
" Q g& P( W7 h" P3 \3 H* zDurable complete molecular remission of chronic myeloid leukemia following6 ]6 H3 G8 ^6 d1 @+ d6 Z
dasatinib cessation, despite adverse disease features.
, B1 L L$ ^1 cRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
8 x/ p0 o z% r+ W2 n% nSource8 m% w, F% l) b; r" D2 P0 ?
Adelaide, Australia;
+ I' U/ B; e- w+ F: A: D* d6 Q) T; c) [" F: X
Abstract
( [& k4 Y5 y3 F/ X0 [7 k1 `4 b2 nPatients with chronic myeloid leukemia, treated with imatinib, who have a
7 @6 ^8 B" t: ?! jdurable complete molecular response might remain in CMR after stopping
, l1 V( |( W9 [6 f9 s8 Gtreatment. Previous reports of patients stopping treatment in complete molecular8 l! [6 a9 k# L
response have included only patients with a good response to imatinib. We2 ?$ J" y' A! Z
describe three patients with stable complete molecular response on dasatinib L4 c0 ^" g' Z% H% f
treatment following imatinib failure. Two of the three patients remain in: t8 H0 b3 }$ _5 h# \
complete molecular response more than 12 months after stopping dasatinib. In
0 F6 A( T+ N) V& b( W7 e- Ithese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 c( L* H% p7 q }. {+ P# B
show that the leukemic clone remains detectable, as we have previously shown in% ?1 U% X1 _1 C$ `& f
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as' m5 \! x- G! F( z
the emergence of clonal T cell populations, were observed both in one patient
6 O. j3 r3 n r, K1 I: S3 awho relapsed and in one patient in remission. Our results suggest that the
/ E& i' G% G/ Y( Ycharacteristics of complete molecular response on dasatinib treatment may be
$ f% L [5 }' m Z3 t! _ T4 isimilar to that achieved with imatinib, at least in patients with adverse
% O2 E! Y4 ~% }. Tdisease features.
6 R9 \) V3 s4 y: } \& V |