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. E+ H2 _( V' T; 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。
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; {4 n. F! W p& |7 ]作者：来自澳大利亚
" a v, U$ R) V4 ^. J来源：Haematologica. 2011.8.9.
) S1 W, Y3 h; j# eDear Group,
9 R! ]2 C" e" ^0 S! l5 V/ |2 ^3 u# N
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
3 f, U% q7 W6 h/ Mtherapies. Here is a report from Australia on 3 patients who went off Sprycel. U' c) e! @3 g3 ~- I9 R8 o/ I
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
1 k9 P6 a5 o+ D, \/ R+ H" M/ P7 R" ^1 Fremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel3 ]0 ]0 I, K" M0 d
does spike up the immune system so I hope more reports come out on this issue.
- ?) I. h$ j* Q+ k; H0 f0 l& w- o7 l3 y1 x2 Y/ s
The remarkable news about Sprycel cessation is that all 3 patients had failed
* H: ]/ k1 {5 B" FGleevec and Sprycel was their second TKI so they had resistant disease. This is6 d x& L& h: i" A1 O2 U, |' |6 n0 U
different from the stopping Gleevec trial in France which only targets patients( z' D% V( Y7 D4 O! }2 {
who have done well on Gleevec.
4 T3 n& [6 D1 D; a
% G6 ~5 M) R; r" x$ X4 K$ UHopefully, the doctors will report on a larger study and long-term to see if the
" y2 x; @/ Y0 b0 c7 p4 y5 H6 Nresponse off Sprycel is sustained.: \" D' }5 l6 F1 u& S9 x7 A5 e* F9 w
' v1 K& ~% N7 l" dBest Wishes,) n* B& u* m8 o: C. z) ^8 P
Anjana+ I9 h' }5 C$ n+ n V: g' Y1 Y
0 K: O& `- h# d6 d+ Y3 G4 D
4 }$ O" r: D+ i: \9 ~
1 V3 s4 Y+ Q1 S% r
Haematologica. 2011 Aug 9. [Epub ahead of print]
& w# P5 B' f: v3 k( C9 v7 G3 n" s/ \Durable complete molecular remission of chronic myeloid leukemia following
8 m) I) [6 Q- Y0 N) ~dasatinib cessation, despite adverse disease features.
0 N. e4 q* ]( k0 | I( e7 O* ~+ GRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.7 a [* b T9 Z/ N6 } h4 N# S
Source3 t* h" @! F8 \9 E7 o, F3 l4 B
Adelaide, Australia;! i& u4 n$ ]+ q& F( x
# Y! m l5 C9 W0 B3 @* U. z1 }! lAbstract
$ k+ E# a `$ W- L! o( PPatients with chronic myeloid leukemia, treated with imatinib, who have a
; Y6 h$ q% Y- |* sdurable complete molecular response might remain in CMR after stopping& z; l( h& Z. E* \; w+ l: j0 {
treatment. Previous reports of patients stopping treatment in complete molecular& f; x6 b7 A5 g( ?/ [' I( E
response have included only patients with a good response to imatinib. We
, g. ^9 k% \7 Wdescribe three patients with stable complete molecular response on dasatinib
4 S1 H' s: A& Utreatment following imatinib failure. Two of the three patients remain in
6 m V! y: k4 _$ X# O+ Ycomplete molecular response more than 12 months after stopping dasatinib. In) g# l5 _7 }3 K; E
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 g2 g( g) o- X
show that the leukemic clone remains detectable, as we have previously shown in f4 c! n- F" P' f
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- d$ g- m; v+ p' f! k- K: w# ?
the emergence of clonal T cell populations, were observed both in one patient; R% \1 y* [ Z# \; `- I C
who relapsed and in one patient in remission. Our results suggest that the
( Q' \7 m- M9 ~, l2 Mcharacteristics of complete molecular response on dasatinib treatment may be3 u% `+ j' x* {/ C4 z
similar to that achieved with imatinib, at least in patients with adverse8 o. j; `+ K L x4 {
disease features.! V: h7 X' i/ ^" N
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