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。
0 F# C* F3 G) {% U1 W( w3 |) ^4 E' w 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。$ `& |. k1 ~5 s' j4 _. J# [4 ?
2 \- q8 @0 v5 Q- _作者:来自澳大利亚2 r. y1 `% r9 ?- r% y$ M! K
来源:Haematologica. 2011.8.9.6 R: E+ Y8 N+ a
Dear Group,
7 L/ t- K' S# t5 r0 O# O! T9 f
9 W6 e4 ?+ |! t7 A! @# QSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
1 u$ e: ^6 v9 Z; j6 |! k& Ztherapies. Here is a report from Australia on 3 patients who went off Sprycel( w9 r* a2 @: F
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients: A) q5 R% M; Y8 t; i
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel- e. C1 e0 k& a @5 a3 K
does spike up the immune system so I hope more reports come out on this issue.5 ]* A$ k: x/ a# A5 K9 f6 U0 G
# F9 q* t3 [* @/ n+ W! FThe remarkable news about Sprycel cessation is that all 3 patients had failed
/ j3 p4 w' P+ ^% j$ E8 \1 U; U7 QGleevec and Sprycel was their second TKI so they had resistant disease. This is& ^" d; T) Z7 |' R; O; \( L
different from the stopping Gleevec trial in France which only targets patients
r" ]% ^# J$ M# _$ Nwho have done well on Gleevec.
1 H- M/ E" c! N8 r3 e
: E6 C0 C" a& YHopefully, the doctors will report on a larger study and long-term to see if the, `. r' J+ [% A; w2 T: ?$ C
response off Sprycel is sustained.
( q/ |( G/ G4 W# Y: w# V% F
8 x) R+ D/ [; ^7 E2 f% |4 ]Best Wishes," @/ L1 D7 ?3 A0 h, p
Anjana: Y& ~! D% ?" T; t5 p
; V1 S m; `0 E9 q! K* @+ [
9 n. L: p" l* |, o( U+ a, j+ E3 r/ U+ S* m1 g& c$ _
Haematologica. 2011 Aug 9. [Epub ahead of print]5 ~/ F7 v( @7 A1 [5 S7 j* b# l. o
Durable complete molecular remission of chronic myeloid leukemia following0 ~, C' {' H& [$ Q* {0 O0 p3 j
dasatinib cessation, despite adverse disease features.# X% k/ X" B' S& ~) u
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
6 S. q) O+ j6 d8 h: RSource
' s7 v" h U3 N" k5 ZAdelaide, Australia;
7 S4 Z* H! w1 [. s4 n4 a( f' j: B0 ?7 i5 g- j8 _
Abstract
* ?6 B6 K/ b8 l1 F* fPatients with chronic myeloid leukemia, treated with imatinib, who have a
0 m B' a% [# v0 Zdurable complete molecular response might remain in CMR after stopping l7 B6 F5 i1 k2 b! x
treatment. Previous reports of patients stopping treatment in complete molecular
5 l& Z6 z& A* x+ kresponse have included only patients with a good response to imatinib. We
+ R+ R2 H" M$ qdescribe three patients with stable complete molecular response on dasatinib
0 ~4 F* J4 W1 |6 J+ s. `treatment following imatinib failure. Two of the three patients remain in
5 N( }" Q$ I: u1 D9 z5 a: v1 Pcomplete molecular response more than 12 months after stopping dasatinib. In
, r( D- ?9 p- u" A8 D) `3 athese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* S& ?% x! I, v# J3 Ishow that the leukemic clone remains detectable, as we have previously shown in' m. w2 z; a4 Z8 L3 b, Z
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
4 R& |/ r' y- U$ Athe emergence of clonal T cell populations, were observed both in one patient
# `6 U) c$ |- ^6 U/ H0 [9 P4 Twho relapsed and in one patient in remission. Our results suggest that the- J+ _6 f+ b; D6 v! P
characteristics of complete molecular response on dasatinib treatment may be
" i. o$ y- ` X$ s7 j5 _- ssimilar to that achieved with imatinib, at least in patients with adverse
# j' i" S# j, `/ `disease features. X5 ^! T8 _' ^1 n
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