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。
$ O0 w$ Q5 e+ M: p( I) A5 Q, { 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 Z+ T7 ^4 c$ t% e ) V1 {6 z! w, F: O7 G' i" u) s& |
作者:来自澳大利亚; P: I. @5 q: H7 u
来源:Haematologica. 2011.8.9.; o8 @& [. O* u; B, v
Dear Group,
' b! Q- ?) i. O6 |1 m# T8 P; [& M) @9 [
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 _3 h) U4 U `( o9 j
therapies. Here is a report from Australia on 3 patients who went off Sprycel
6 V/ A x D5 X- }' F1 Qafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients o' A, ?0 E2 T6 O/ L+ G; y2 B$ J
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel% r, Y- g3 W+ u* S0 N4 T. R
does spike up the immune system so I hope more reports come out on this issue.
?- @' c6 a w5 X$ N+ r# a4 Q3 U! V; B6 Z/ V" m- \5 S2 [
The remarkable news about Sprycel cessation is that all 3 patients had failed# U, ^) S2 S& ~
Gleevec and Sprycel was their second TKI so they had resistant disease. This is/ x$ L! ?1 [- K% Z/ X, R( @- o! H( w2 C
different from the stopping Gleevec trial in France which only targets patients
0 \3 d- M( {7 i* Y1 |! Zwho have done well on Gleevec.8 c( r/ R; ]+ }. }- @# W
" N% U2 e& }$ \1 D- W6 FHopefully, the doctors will report on a larger study and long-term to see if the* F. B* E& \1 c+ w; u
response off Sprycel is sustained.
, R2 K! o, G$ d$ I3 C$ o
' B. h+ Y8 `# n1 I& p! [Best Wishes,0 _; e2 j5 W. l3 p& R
Anjana `$ R) {5 Q' M6 F, j7 N5 _
: K+ M, i" ?" h' |; ]2 `: j$ u8 z# B+ K, _% `# y: h# v- l
$ S4 `" ]$ P9 M, k% U8 IHaematologica. 2011 Aug 9. [Epub ahead of print]
! ?1 B& o6 S. a( ]Durable complete molecular remission of chronic myeloid leukemia following4 u! ~; ]1 b& b1 J. `% F
dasatinib cessation, despite adverse disease features.
8 w9 W3 `6 b: W/ S6 M, pRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.8 } p- n0 v. T
Source2 S# I0 T4 ?$ a& C
Adelaide, Australia;: l) V5 ]( N0 e# E1 K9 a1 w
3 \1 E0 y! @! |0 R
Abstract
6 M E/ t1 X3 U2 x% S2 j3 vPatients with chronic myeloid leukemia, treated with imatinib, who have a( c' b4 p* `! p! B r( s) w
durable complete molecular response might remain in CMR after stopping- }8 I6 S4 r/ j: C
treatment. Previous reports of patients stopping treatment in complete molecular
& Z9 u$ w& L# k0 l) vresponse have included only patients with a good response to imatinib. We' ?0 f+ M/ d8 O1 ^2 F
describe three patients with stable complete molecular response on dasatinib
k6 z- U9 z' }9 e% m2 H$ p/ ztreatment following imatinib failure. Two of the three patients remain in/ d6 r- n6 w# O0 N; Y5 ~
complete molecular response more than 12 months after stopping dasatinib. In
5 Z( m* H* Y7 l( u4 f1 @these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
% J2 \6 c0 b0 |) u% e5 X, Z9 yshow that the leukemic clone remains detectable, as we have previously shown in: d6 e9 g c; I( N6 Y3 @( u6 T
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 q. M) r1 N- }5 F" x( R
the emergence of clonal T cell populations, were observed both in one patient) V/ O9 b" c3 G4 {) ^$ u7 R
who relapsed and in one patient in remission. Our results suggest that the4 @6 R+ t+ w0 X3 A
characteristics of complete molecular response on dasatinib treatment may be
1 C' ^ c2 s& ~, Y" i y; Q+ s! I5 hsimilar to that achieved with imatinib, at least in patients with adverse: G+ ?. @5 l" e6 T U! @
disease features.
5 o% j7 S: \* J/ y1 _. F |