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。
# Z3 U1 c: B3 B2 B( U- 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。4 H- K% q1 o y d5 |, j9 O
6 [1 B) B- P/ L8 K9 ^3 q: g! ]* Y作者:来自澳大利亚5 T, E: Z- U, c# G( ]! E
来源:Haematologica. 2011.8.9.
: Q+ A4 d/ Y: L: D8 N; fDear Group,; \9 T1 g: P7 c, ^
% k0 K, ?' E4 N4 ^- X4 |) fSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML Y1 l1 S$ h2 b2 `9 r# Q
therapies. Here is a report from Australia on 3 patients who went off Sprycel; M4 `/ R- J V4 h; c5 N
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients+ m8 w9 ^9 c! s1 _5 ?( i4 K5 w* I
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 J, S( @0 Y5 X2 G
does spike up the immune system so I hope more reports come out on this issue.
4 S9 e; q4 k0 M1 V- o( t) Y. S8 P1 N* ]4 X
The remarkable news about Sprycel cessation is that all 3 patients had failed0 F% x# e0 J1 w) t. q
Gleevec and Sprycel was their second TKI so they had resistant disease. This is4 O. q+ J* U% r3 K8 K
different from the stopping Gleevec trial in France which only targets patients7 k( u5 V9 {; y7 q
who have done well on Gleevec.; u* W/ [2 x; X6 `# N! n
, L) W+ u1 G& }1 J
Hopefully, the doctors will report on a larger study and long-term to see if the: d" P- Y+ W& ?# F9 T
response off Sprycel is sustained.( z8 h" D+ a. \& m# z$ Y: h
* J' [( I5 z4 ^* a
Best Wishes,
+ ?7 q+ P- P0 U* K$ ^# K. ~! F) S& wAnjana
2 R; j: |& l8 k& I- O9 a1 U. _! F' e- O) a' y- b6 V' O) L+ u2 w
. K/ ?; c+ |8 m9 M' r* S& H
6 n& C9 C K E3 HHaematologica. 2011 Aug 9. [Epub ahead of print]
" C8 S) b- K; { B. }% v9 X! uDurable complete molecular remission of chronic myeloid leukemia following% b7 Q5 W4 Q) P4 d
dasatinib cessation, despite adverse disease features.; x1 z; v7 E" c2 u. p* q
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
. q. ?) M. i. T' t' m5 oSource: W! N A9 T L8 c
Adelaide, Australia;
, _6 x* A' L) Z/ F- p6 V( P
( u+ X, C5 H& O i; ?+ ]Abstract! [: v/ M/ l' b0 J7 S
Patients with chronic myeloid leukemia, treated with imatinib, who have a
, J5 o% @6 N' I" K6 udurable complete molecular response might remain in CMR after stopping& M9 p+ U; j3 i$ b! l& k
treatment. Previous reports of patients stopping treatment in complete molecular: f6 t d! P+ I& C- E) m& T
response have included only patients with a good response to imatinib. We
* n8 W2 j" ? R5 u- ^" z4 \describe three patients with stable complete molecular response on dasatinib
; S. C2 N2 p( Vtreatment following imatinib failure. Two of the three patients remain in
5 k' }( Z+ r% |4 o% dcomplete molecular response more than 12 months after stopping dasatinib. In
' x# |" m7 k4 Ethese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ ]7 s2 Q- _4 U$ n6 p8 u7 V; F9 m$ L
show that the leukemic clone remains detectable, as we have previously shown in
7 U; M7 S5 z1 ~; F. Eimatinib-treated patients. Dasatinib-associated immunological phenomena, such as& K" W0 X/ B7 K# z/ r; z
the emergence of clonal T cell populations, were observed both in one patient
% u( v) d1 W% s+ h* z' Vwho relapsed and in one patient in remission. Our results suggest that the# n/ M: R5 h+ H: j) {& k
characteristics of complete molecular response on dasatinib treatment may be& s% U1 v* a' y8 K. m' D
similar to that achieved with imatinib, at least in patients with adverse
( f% C- i" N7 B6 S2 ?$ gdisease features.
" a( V$ N( V, b# c! t |