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。
, j: v9 |% b6 j1 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。! r1 E4 t) W9 ^1 ~
3 S$ k1 Y9 s* ?3 }作者:来自澳大利亚
9 C2 t9 q9 [1 f% Q来源:Haematologica. 2011.8.9.
3 [+ f. w1 o2 UDear Group,
6 ~+ F1 A- B5 _% j3 w6 S" _0 \2 Q6 D* @
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
" E/ _: N* P3 I0 b$ Utherapies. Here is a report from Australia on 3 patients who went off Sprycel
1 f$ h( m: t. S6 A) L6 v: pafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
. i" D* s$ x% f0 gremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' l }: l2 A% y/ G1 L) `1 E% L$ m, ^
does spike up the immune system so I hope more reports come out on this issue.
1 U! b% O% d9 p/ u! D, @( ?2 V7 r) d# l. ~0 p9 A+ L: | j
The remarkable news about Sprycel cessation is that all 3 patients had failed0 c; A8 D* H/ h4 {: m8 E
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
" Y; a4 u. p5 N! U t! ydifferent from the stopping Gleevec trial in France which only targets patients
9 b% x2 Y1 E4 {* S! a; _& ]" t2 t% ?who have done well on Gleevec.
" V5 o% }8 }2 X& } F
5 B0 H+ e) [- P8 ?Hopefully, the doctors will report on a larger study and long-term to see if the
M! Q! W( \8 H6 }, [; `response off Sprycel is sustained.
8 f2 p# V) W6 u9 z
4 u) h" j$ w/ y7 z9 ZBest Wishes,$ |* i, ]3 W7 i: v. ^) _
Anjana
; C& r: L$ @, _- m$ Q# w1 Y* S/ I/ H" a3 d: M% o
$ D* O+ w: C9 g0 ?
. K0 d4 Z: \! I& cHaematologica. 2011 Aug 9. [Epub ahead of print], I8 x/ y ~+ A% P' O' r- g. u( |
Durable complete molecular remission of chronic myeloid leukemia following
g) D1 @& e: ?/ y6 Z$ p3 j7 m1 kdasatinib cessation, despite adverse disease features.
- Q" c# @4 @; R0 P( }' P8 @Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.* J$ L6 M- X( P
Source- p/ H4 p! }5 R; a h& V- h& @
Adelaide, Australia;
1 l' D* Z* h% i6 I; S2 i! O/ E/ y8 u% E U% s+ j: j3 b, {4 v: [- H
Abstract
; A$ a' ?! g5 l: q9 M6 Q$ ZPatients with chronic myeloid leukemia, treated with imatinib, who have a
9 B% ?- D8 Z# r" mdurable complete molecular response might remain in CMR after stopping
1 [$ i* a+ R' ~2 u: t9 S5 P! d" G" C9 Ctreatment. Previous reports of patients stopping treatment in complete molecular% i j4 ~2 F3 |3 C2 X4 x0 e
response have included only patients with a good response to imatinib. We& {2 ~4 t3 y4 n0 T7 R5 |
describe three patients with stable complete molecular response on dasatinib
! D: r# w) w0 ^0 ~treatment following imatinib failure. Two of the three patients remain in
# S% G' c6 ]2 z5 r; r+ Ncomplete molecular response more than 12 months after stopping dasatinib. In
* V. \/ W) W. r* l, Gthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
2 i! s7 ]- G. f: sshow that the leukemic clone remains detectable, as we have previously shown in9 l* _. p8 y. A
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- B# e- `5 i3 R% E, O8 r; b
the emergence of clonal T cell populations, were observed both in one patient$ s5 T2 U$ j: g5 a& w2 N4 I
who relapsed and in one patient in remission. Our results suggest that the5 H6 n' |- ]7 f7 k/ _7 J, y
characteristics of complete molecular response on dasatinib treatment may be
7 x- `% [/ e. a8 rsimilar to that achieved with imatinib, at least in patients with adverse" b5 K4 I$ v3 n" N( w+ Z3 P
disease features.0 N8 f- E: q: Y% q ^
|