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。
8 m4 ~' Z! W8 c4 G3 F7 r 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。
# E2 k7 t7 y5 h
# {0 s$ \% l) P9 u作者:来自澳大利亚
$ k$ [5 E" Z8 I! g) h% F来源:Haematologica. 2011.8.9.; a/ [- T, {/ F x1 c1 {& |
Dear Group,
. C2 I) V3 R+ a& K6 n* y" B( B
. S6 P. s8 D0 C. [Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
) \3 _9 V5 P" Ftherapies. Here is a report from Australia on 3 patients who went off Sprycel
$ z* H) Y* f; J- ?: vafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
* i( d* {+ ~. Hremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel3 f3 V J4 p9 w5 z$ [
does spike up the immune system so I hope more reports come out on this issue.; W+ a( W( x5 R" @% X/ G
& ^' y0 s, A/ B5 @
The remarkable news about Sprycel cessation is that all 3 patients had failed
# ?1 i- r- X1 d _" U; i: [Gleevec and Sprycel was their second TKI so they had resistant disease. This is
3 I6 e8 X, v7 ~+ Tdifferent from the stopping Gleevec trial in France which only targets patients, q8 Y& _5 G3 c$ g5 J5 g
who have done well on Gleevec.
7 m' }7 G8 ?6 z$ ^+ p2 m9 q3 u! P" U' v! I% Q" |
Hopefully, the doctors will report on a larger study and long-term to see if the
6 v) N+ B. C: C& b3 u1 j2 cresponse off Sprycel is sustained.0 b# X* k4 X0 @$ i. U8 w4 }4 t
, P% ~ I" r* y z; O$ UBest Wishes,
f$ U0 x2 ^& E8 Y% }6 J2 ] C: bAnjana
0 g; P5 B0 P: J2 l
: Z( Z& W8 B4 ?: E, `3 K8 S- B6 y: A, |* T
2 k# M7 C j; u' P4 i
Haematologica. 2011 Aug 9. [Epub ahead of print]
* d9 C; l! }! D) h! C" SDurable complete molecular remission of chronic myeloid leukemia following
; \: h1 t3 D; X; Y: P) E$ bdasatinib cessation, despite adverse disease features. }0 Z% ^# C& I' z% n4 W, o
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
; l0 B# j0 Z. Q+ N/ `3 pSource; ^7 v/ H2 T* k/ s
Adelaide, Australia;0 b4 Z# U1 V7 f( H' y, \1 O
8 u1 y! v5 v" B! V6 `( e K) w
Abstract
. f& r, ?1 Y4 N" HPatients with chronic myeloid leukemia, treated with imatinib, who have a
* L) W8 B! P$ O* Rdurable complete molecular response might remain in CMR after stopping
6 S3 C! [/ G' p l* ttreatment. Previous reports of patients stopping treatment in complete molecular
, P/ Y; }0 s* r4 s) Jresponse have included only patients with a good response to imatinib. We8 h# G$ n7 g A" m- L# [1 J
describe three patients with stable complete molecular response on dasatinib: E9 a q0 k$ L, h8 {! r
treatment following imatinib failure. Two of the three patients remain in1 v! }5 \ \: A* {/ X
complete molecular response more than 12 months after stopping dasatinib. In
3 ^4 j& y2 R: S+ Athese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
9 V# ~/ A2 z4 V& P4 u# l$ W+ K7 Ashow that the leukemic clone remains detectable, as we have previously shown in
0 r. d# T6 T! k( R# Y, Mimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
1 U' x$ Q; u/ K8 K' y" K3 lthe emergence of clonal T cell populations, were observed both in one patient6 M/ p7 _* \3 j
who relapsed and in one patient in remission. Our results suggest that the
0 g4 _' ?1 Y- e B0 [& \' P2 k; Scharacteristics of complete molecular response on dasatinib treatment may be
/ j. V1 x- n4 h! k* }. a6 ksimilar to that achieved with imatinib, at least in patients with adverse# A$ c. h& W% D# l) j$ m5 k' ^ O& x
disease features.
% y8 w6 F% ]7 r5 C |