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。
9 Z$ ]) A" y6 V1 s4 n6 q$ y 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。
0 X8 w" r6 K- y& F, C 4 \6 M6 R. c+ S) J
作者：来自澳大利亚
2 u& L; b: A/ ]9 i, \/ E来源：Haematologica. 2011.8.9.
" x+ ~' x4 z, s- uDear Group,
) ]+ B$ J6 Y4 _- k% m; M! A# ?
1 K5 \8 f( d2 N% P; T6 BSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML: Q) t( m i8 W$ O0 k6 R+ G* p* E) @3 w
therapies. Here is a report from Australia on 3 patients who went off Sprycel
% ?9 [* ]9 l- R* c8 S) W9 aafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients5 |! j4 W I' }; I$ G
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
R6 C% p4 \4 t* U& `does spike up the immune system so I hope more reports come out on this issue.
% K2 m# Q3 g, k% J1 K" Z k) P9 z, x1 p) y8 x3 J. K9 k
The remarkable news about Sprycel cessation is that all 3 patients had failed
+ w9 \' H: K# z3 [Gleevec and Sprycel was their second TKI so they had resistant disease. This is
# A0 G/ h/ a' D/ s- adifferent from the stopping Gleevec trial in France which only targets patients
, V% y3 |# E' B: |- d. `; Gwho have done well on Gleevec.
9 |' u9 j. N1 S* [( O2 e, ?3 r
, ^6 ?0 a. x- p% F) \Hopefully, the doctors will report on a larger study and long-term to see if the- {8 ]9 O( z! \+ V2 D' V4 }
response off Sprycel is sustained.
, \; Q9 m% G& X B, M8 v" d$ _6 u% e' h8 o, g
Best Wishes, ^# K9 C S" a6 j* x. S
Anjana
2 {- C' Y8 ^" m s
5 }, x- Q# {+ D8 `& p5 a: ]% [# N/ {+ K! M1 d" \% {, B5 ~4 Y \
# D- X1 r+ X9 B0 t3 r
Haematologica. 2011 Aug 9. [Epub ahead of print]
! Y* I ]! V' a8 rDurable complete molecular remission of chronic myeloid leukemia following
4 a0 g& y5 U; b9 p/ Q6 P0 [% ^dasatinib cessation, despite adverse disease features. o9 }6 x, z& V& ` \
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
& q8 o0 k2 K1 i0 dSource
! J" ]. q/ i; A) L0 {0 Y8 ?9 BAdelaide, Australia;
2 A6 c F. X5 b$ B X, E" H. W- p
1 U h6 y2 V. k4 F* gAbstract
# h! q5 d; B4 _3 oPatients with chronic myeloid leukemia, treated with imatinib, who have a
' ?; e( d. e/ w- q7 S" i- ddurable complete molecular response might remain in CMR after stopping
9 B. J( o4 S4 D2 a+ h: @treatment. Previous reports of patients stopping treatment in complete molecular) r* p) s: l4 }8 ]3 m1 E7 f
response have included only patients with a good response to imatinib. We
+ h) V/ z% a/ zdescribe three patients with stable complete molecular response on dasatinib
L& [0 L8 A& \' X( g8 Z# y1 }( Jtreatment following imatinib failure. Two of the three patients remain in8 j1 d) B) Q3 D( Q2 u( s
complete molecular response more than 12 months after stopping dasatinib. In+ j; u- h/ }8 b
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to2 G1 g2 L( c4 J) p
show that the leukemic clone remains detectable, as we have previously shown in' |0 c% g) I- P$ N- m, k
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as& c# ?. ?+ t& T9 [6 \
the emergence of clonal T cell populations, were observed both in one patient" p$ x5 F0 Z/ o/ Q& t6 D5 R
who relapsed and in one patient in remission. Our results suggest that the
2 E6 X% F/ d6 s# A" Y+ Q- s$ Gcharacteristics of complete molecular response on dasatinib treatment may be
H( |& |: s. C5 t0 I- R$ Fsimilar to that achieved with imatinib, at least in patients with adverse: V @0 s, W" b7 e
disease features.
% Y3 p# Z/ i; C& z |
11011102001537 )
显身卡
