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。
2 ~( Y) \$ N6 G: v q( F' o 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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2 l+ n2 S, P) \) u# ~作者:来自澳大利亚
+ Z/ @# q! n7 \5 i1 e3 W% g4 A来源:Haematologica. 2011.8.9.
; J) E2 S$ u6 V& d* xDear Group, Z% X l: T( W4 M. r1 _
: Q N/ U$ z# |! g) z9 e2 FSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
3 w; R/ u- ~7 a. A4 w" \7 vtherapies. Here is a report from Australia on 3 patients who went off Sprycel0 l' {5 `5 ~: O: P2 M
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients$ I/ n0 e; _0 m& R
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel0 ~% {8 `& ?; e# K( ^0 M
does spike up the immune system so I hope more reports come out on this issue. E$ _6 x F" x: ^: x2 |
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The remarkable news about Sprycel cessation is that all 3 patients had failed
5 x6 ^" h: M! ?8 V A' ^# MGleevec and Sprycel was their second TKI so they had resistant disease. This is
$ g4 p5 @+ x* c$ ?* B e: v* n% G6 Sdifferent from the stopping Gleevec trial in France which only targets patients, P$ |5 U9 v. J2 `
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
5 c$ Q* ]. u6 sresponse off Sprycel is sustained.3 A" i E: m! v, _
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Best Wishes,
8 o ^/ ]/ X! `Anjana( ^5 G/ H/ Y. c, A e& F% j
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8 M! L; \, Y4 b# G s2 n( n& T7 L- l! {, g9 ^
Haematologica. 2011 Aug 9. [Epub ahead of print]
+ ?6 o4 w7 z; O" D1 D+ V2 ~/ ]Durable complete molecular remission of chronic myeloid leukemia following5 H6 B0 I0 c& c* l* x6 {
dasatinib cessation, despite adverse disease features.
1 L% F8 f( c) BRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 S7 B0 |' P) a5 L" |8 @7 V# F
Source1 e$ {8 Z3 {8 w3 H
Adelaide, Australia;
: n5 U$ B0 C' [- }
5 y7 t& v- e+ ]Abstract1 h' z z$ U! W- L5 k' @1 ?+ H
Patients with chronic myeloid leukemia, treated with imatinib, who have a! M9 n# e1 S0 D. f$ }. b8 x( e
durable complete molecular response might remain in CMR after stopping# A5 ]; d8 F, k- s: w6 }/ Y5 G
treatment. Previous reports of patients stopping treatment in complete molecular2 L6 i* ^" g" {' X, m1 J
response have included only patients with a good response to imatinib. We$ s ]$ o: R( d. Z9 F- N3 T4 r4 Y
describe three patients with stable complete molecular response on dasatinib9 s& f$ X( t& t8 `, I
treatment following imatinib failure. Two of the three patients remain in: A6 ]' Q' E+ M9 X Y
complete molecular response more than 12 months after stopping dasatinib. In7 ~ M V; |/ Q0 N. C9 U$ F
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to0 l0 {; J0 u5 D) R) H U5 P0 L
show that the leukemic clone remains detectable, as we have previously shown in
2 G6 p) ?% j" iimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
4 @' b0 E6 C: wthe emergence of clonal T cell populations, were observed both in one patient
3 t% u6 I2 ~8 k6 b Awho relapsed and in one patient in remission. Our results suggest that the
9 ~; b# X5 `) tcharacteristics of complete molecular response on dasatinib treatment may be, u" u9 w8 c! J* q
similar to that achieved with imatinib, at least in patients with adverse
/ R% P8 x8 I% rdisease features.: b/ q/ |- \7 x5 G5 ?
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