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。$ g6 f4 H) e0 ^6 ~1 F) Y. U
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。
& F0 g. R: d8 _4 j" m2 i0 U
7 L/ Z& v+ P4 ?3 ]1 [作者：来自澳大利亚, [ S( N& p7 r; [% l/ V; L$ L' [
来源：Haematologica. 2011.8.9.
( G3 Y1 v0 e: s1 E7 X: M3 IDear Group,
" b5 E; ~' y1 o) `' v. C: `' E8 t# T: h9 z8 {
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML5 I$ Y+ y8 Y9 o/ A S
therapies. Here is a report from Australia on 3 patients who went off Sprycel6 a9 Y, }) e$ I3 t- q5 v
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 R; m2 L8 S+ f' ^* sremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
( p( ?/ R. e3 D }2 c- Z; Ydoes spike up the immune system so I hope more reports come out on this issue.
, A Z$ `4 X: v5 S0 G9 V) l- ^; ~- e" e- E7 E% C, D9 \
The remarkable news about Sprycel cessation is that all 3 patients had failed, q8 l, N! X4 Z/ g; n E
Gleevec and Sprycel was their second TKI so they had resistant disease. This is+ O8 Y# L8 P; x& U
different from the stopping Gleevec trial in France which only targets patients
3 T5 w( B# b' q2 Uwho have done well on Gleevec.
( k; o& m& g9 z7 u% B) G( \8 k8 k, t+ o
Hopefully, the doctors will report on a larger study and long-term to see if the H R4 m# [0 p+ I
response off Sprycel is sustained.3 W& R! l% O) l9 k
) u6 w" h2 `/ ^/ F4 M+ N. eBest Wishes,. Z, h/ C/ R) C2 I4 a
Anjana5 x# R" a: q3 g
& |( }4 q7 P$ u& N" F$ `6 t$ L
9 P' ^) S# x. T" {2 ?$ T. q: j
9 |2 i O% n+ x; z9 N* _. d4 r
Haematologica. 2011 Aug 9. [Epub ahead of print]' C4 R. F1 K$ `3 Q) I& q
Durable complete molecular remission of chronic myeloid leukemia following
/ }# }4 v; \) r% Bdasatinib cessation, despite adverse disease features.) t V s3 a2 ~' r" z
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
% s& Y) o8 J; @; W, y+ U4 K( _5 HSource
) z* c$ l% s9 n) G* w' ~Adelaide, Australia;
: ?0 D W8 k; Q1 ^
1 `! R" \) h- T! G: aAbstract
% D8 O3 i) ^6 J3 ?* o9 xPatients with chronic myeloid leukemia, treated with imatinib, who have a7 ?$ s+ f8 F5 u2 I
durable complete molecular response might remain in CMR after stopping
, _+ h% Y4 g: O! S2 C) Z$ Rtreatment. Previous reports of patients stopping treatment in complete molecular
% c7 Y3 O$ J! k* ` z2 yresponse have included only patients with a good response to imatinib. We
3 B, t) [8 E# b; Mdescribe three patients with stable complete molecular response on dasatinib; c, g7 a2 i, A, Y' @: r6 s9 e
treatment following imatinib failure. Two of the three patients remain in
# Z* r6 s* F/ t {. q' g% Gcomplete molecular response more than 12 months after stopping dasatinib. In% \# O! }5 w9 G* E5 c- x5 H- _
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
, V, S) a1 y# k. I" E, ~show that the leukemic clone remains detectable, as we have previously shown in: Z7 c$ B% }7 S2 L/ O+ F, _ \
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
: W6 K6 J; A' e( h3 hthe emergence of clonal T cell populations, were observed both in one patient
* P6 a$ ~8 G; W& M# vwho relapsed and in one patient in remission. Our results suggest that the6 m @: Y4 H, G6 d7 R
characteristics of complete molecular response on dasatinib treatment may be1 q; K6 f7 h( @$ x
similar to that achieved with imatinib, at least in patients with adverse: P/ w8 S ?1 `5 U+ L6 m0 Q
disease features.
* r+ K/ k! E7 H6 W5 i+ @! Y |
显身卡
