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。
1 \; m8 ~/ B* E 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。: Z1 v f9 r8 f: f" f7 c Q
, [9 L% u4 n: b6 Q作者:来自澳大利亚
. O1 _: T% c, `% [/ i! q+ A* [! a) Z来源:Haematologica. 2011.8.9.
; U! C; v9 A0 e5 xDear Group,3 c W+ F* k" V0 H8 m; I/ v
2 s0 Q9 I$ M0 F* G- [6 t5 y3 k( B
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML# n) S! I1 R; ~5 u) Y0 `1 J
therapies. Here is a report from Australia on 3 patients who went off Sprycel! J, f. v, t/ W' ~5 c
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients& ^* s2 n! s5 g/ ?. Q
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel9 L5 z. Z; c `% h- H/ r% P; L
does spike up the immune system so I hope more reports come out on this issue.( y, Q1 }' k# |7 q6 j* f& u
/ j5 m% v8 P# {& R5 q' _The remarkable news about Sprycel cessation is that all 3 patients had failed! J7 O9 g4 u* H! {
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
# C2 p2 T G. {; ]: F3 B& R8 }different from the stopping Gleevec trial in France which only targets patients
: }( q; p$ v( O' B3 l- T7 O7 r2 Twho have done well on Gleevec.2 ]! v, O( \& n7 U+ u
2 y8 H+ Q+ v' F; U$ k+ e' j F
Hopefully, the doctors will report on a larger study and long-term to see if the% L& j( p. R9 v5 b
response off Sprycel is sustained.
0 `. H6 q( R5 q Y. S5 _ v- W! Z8 a2 @ G3 d7 I! w
Best Wishes,
# C7 N- I! o( y. fAnjana2 I- f3 s$ o9 a7 u6 ]# C" l
' h9 Q5 r- x0 u' I1 @" a7 O" m
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$ A" e3 z) b' N' E: B1 nHaematologica. 2011 Aug 9. [Epub ahead of print]
- |5 {3 I+ W* k, RDurable complete molecular remission of chronic myeloid leukemia following9 @8 A6 e3 r" R0 ~) K
dasatinib cessation, despite adverse disease features.
. r4 c% k) i- m, y+ vRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.# K$ k# \ Y" Q' G' h
Source4 q* @- l% ?. u5 t, Z7 v( L
Adelaide, Australia;
4 [$ c- J/ k$ v% R& z$ T
) y$ x2 Q8 ?# V9 ?Abstract ~& g% U2 }6 K. D
Patients with chronic myeloid leukemia, treated with imatinib, who have a
* B$ F2 A: }+ J) M1 Pdurable complete molecular response might remain in CMR after stopping
! C* e6 V& C3 V3 {9 W( V8 Vtreatment. Previous reports of patients stopping treatment in complete molecular
2 C" O [+ n( F: e1 |response have included only patients with a good response to imatinib. We* ~$ k6 m2 `& E, T
describe three patients with stable complete molecular response on dasatinib0 |, l! m: E, s( C, X7 H
treatment following imatinib failure. Two of the three patients remain in
+ O+ N8 W" ], \9 q- O. \4 y0 ycomplete molecular response more than 12 months after stopping dasatinib. In
% D7 {5 K3 v- t Sthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to v8 D) r; M p$ a% |% d
show that the leukemic clone remains detectable, as we have previously shown in' N5 U! S/ C) K( C, c6 d, C6 G
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as5 q4 K+ Q8 N+ g
the emergence of clonal T cell populations, were observed both in one patient* x' j9 p, K# F
who relapsed and in one patient in remission. Our results suggest that the
3 \: k; C' Y2 a) W) V1 Echaracteristics of complete molecular response on dasatinib treatment may be2 K1 ?& m& m k* q0 _
similar to that achieved with imatinib, at least in patients with adverse- Q$ a4 f6 d" p
disease features.
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