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% {, N; z/ @) y" n* K. z1 |
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。& o# L! d& q# z8 Q o
/ h( n7 o! J) o/ n3 Y作者:来自澳大利亚' @. a8 k% {: p' w; D8 x
来源:Haematologica. 2011.8.9.
. d' G& o! K, Z+ B& |" [Dear Group,: @3 \& {: A1 f* i5 ]6 G
0 |( q- r. w {. M1 gSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, _" h+ ?. b4 N, n/ c1 ntherapies. Here is a report from Australia on 3 patients who went off Sprycel Z% Z* Y$ w3 |0 R8 y
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients, o) _" C3 Y1 O1 X
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& n7 a. X: O* t2 G0 b& t+ x5 ~6 xdoes spike up the immune system so I hope more reports come out on this issue.2 m; m3 F& e& |, S W( B1 Q: X
( R6 d/ R4 o; B5 F5 _8 MThe remarkable news about Sprycel cessation is that all 3 patients had failed$ y" k, W) v C% ?5 p7 K
Gleevec and Sprycel was their second TKI so they had resistant disease. This is- R& I: e: C8 F8 I6 i. r
different from the stopping Gleevec trial in France which only targets patients
' O. q% p/ y$ C( e5 M2 \who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the, w# \; S6 P0 d4 ~
response off Sprycel is sustained.
% A0 g4 {" h3 ]# @
: Z' k. T! @+ s* QBest Wishes,
6 L$ R$ @: ~. D1 N- H% @5 H& E3 rAnjana
. X" D% H" j! \5 D& Z; u( y% s
2 S, l* e6 q* Y0 B5 U) w q1 {- z( u% f3 ?
/ e! c( A n9 S) H+ \; p; D. N
Haematologica. 2011 Aug 9. [Epub ahead of print]6 T/ U K5 e* E ~, M' R) ~
Durable complete molecular remission of chronic myeloid leukemia following8 a0 _& e" @# t# i
dasatinib cessation, despite adverse disease features.
* k0 x5 { q7 @5 F# E+ aRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.$ Y3 n* W/ v8 f' O( m. r
Source
" Y- G! [4 t" r s9 ~$ k/ O+ n! IAdelaide, Australia;
, v! p6 b# J: S/ k) ?4 {: K# j% c% a& h7 I! k( F
Abstract8 h; N) `, r9 {1 [) k$ O
Patients with chronic myeloid leukemia, treated with imatinib, who have a2 H; J. o' G7 d5 ?; t% B4 M% `4 o
durable complete molecular response might remain in CMR after stopping
; W& P7 P% ?! T- e( N& Ntreatment. Previous reports of patients stopping treatment in complete molecular
4 p2 k( U6 ~+ b6 s4 v" Vresponse have included only patients with a good response to imatinib. We, D0 \+ J9 C, Q! U
describe three patients with stable complete molecular response on dasatinib
% x: o' F$ n; F7 }treatment following imatinib failure. Two of the three patients remain in: a6 s! \- P+ @6 c' p6 x9 |
complete molecular response more than 12 months after stopping dasatinib. In, j. \; Z! l% w5 w8 Z" n- k. ]
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to+ Q$ x" @3 @) ]& d Z' X
show that the leukemic clone remains detectable, as we have previously shown in4 O8 L1 l, r1 g9 j
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
5 [9 m1 D4 B/ V. H; gthe emergence of clonal T cell populations, were observed both in one patient F0 U" t( s" e) W
who relapsed and in one patient in remission. Our results suggest that the
5 \$ N) J4 c3 \) a) J1 \characteristics of complete molecular response on dasatinib treatment may be0 Z/ x) k# q) d. ^
similar to that achieved with imatinib, at least in patients with adverse
6 F: R7 @& q/ ]- @" e) K* |disease features., L! j; H* V; J; r2 Y
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