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。% A9 q7 ? _: c7 s
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。
' F: k; z. B/ a. r3 q/ Z 8 h) @" E o- m- U
作者:来自澳大利亚
5 S$ y- r5 G2 k$ }4 u2 C" c来源:Haematologica. 2011.8.9.' g3 n9 P+ c0 q. Y* H, {
Dear Group,( |$ \/ Z: A* A5 r3 S4 l
, d j) c! K- g2 b: qSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML7 b; W& w* c, \- O1 Q. n, g2 A, K9 J$ h
therapies. Here is a report from Australia on 3 patients who went off Sprycel
2 W% s6 _1 Z. o& b! Hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients0 v2 O- E2 M; W3 C
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel+ c2 E8 T; N @* e
does spike up the immune system so I hope more reports come out on this issue.
8 h& L. W7 Y9 G' K
" w( B1 j( E0 ^- l" U' k5 h. _2 S' qThe remarkable news about Sprycel cessation is that all 3 patients had failed/ p3 j: Y% Z. K1 h
Gleevec and Sprycel was their second TKI so they had resistant disease. This is) n, Q9 ? w& z* Q8 c8 g' w
different from the stopping Gleevec trial in France which only targets patients
. L' y. y0 |4 K# |9 z+ i( J; Uwho have done well on Gleevec.0 t4 \* K& a; h5 g( g# w) \
/ m' ~. }- ?$ M, }5 `8 X( eHopefully, the doctors will report on a larger study and long-term to see if the5 f) H3 ?+ G- }# E6 ]1 n
response off Sprycel is sustained.5 J( e( t; M) l6 ~7 b- G
6 A \( [. [2 q
Best Wishes,
0 d# y* b8 Z! m) b9 o/ L3 ]! EAnjana
; S- y' K7 r/ z/ n& K: v8 l+ \; h5 W& }5 r+ R) b
[2 C6 N. O$ v' i* I. ~6 h; w: p3 H# }3 B% r7 M/ }1 x+ E, m
Haematologica. 2011 Aug 9. [Epub ahead of print]$ z" i( P# t. E) S' _9 o$ p" v" y
Durable complete molecular remission of chronic myeloid leukemia following
8 p" b1 S4 P: ndasatinib cessation, despite adverse disease features.$ f: h# r( ]2 j8 V& B% n0 ~& r
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.% g# ~) m' V- N. N" s8 B
Source) X0 Z( C$ J- P% o$ S( C( @
Adelaide, Australia;9 B/ t: o- U6 ~8 V) _5 }$ L
. i5 o9 K0 ^2 A1 S$ C1 ^Abstract
+ o: X @4 D3 g8 GPatients with chronic myeloid leukemia, treated with imatinib, who have a
# Q# y' j9 `8 mdurable complete molecular response might remain in CMR after stopping
) d7 k/ z M% m |treatment. Previous reports of patients stopping treatment in complete molecular
* O9 Y' ^+ F$ z7 Q: ^: \# U4 Sresponse have included only patients with a good response to imatinib. We$ x& D2 g: |5 S1 Q7 r
describe three patients with stable complete molecular response on dasatinib- N+ z* p3 o% U+ k
treatment following imatinib failure. Two of the three patients remain in
% F, N P- [$ i& X6 K0 Zcomplete molecular response more than 12 months after stopping dasatinib. In
- }! l7 `- e+ D; F# }9 h- d; `these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to% M% G7 a, B- L, x0 K/ ?
show that the leukemic clone remains detectable, as we have previously shown in4 R: c- C, b/ O" c
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ J0 u) A$ Z" o. }& e: ~( _the emergence of clonal T cell populations, were observed both in one patient' d8 i3 Q' G( j1 K
who relapsed and in one patient in remission. Our results suggest that the
/ K e. a* I8 j" h! y6 w$ }: A" C0 ^3 |characteristics of complete molecular response on dasatinib treatment may be/ I! l& ^, B9 W* q, E
similar to that achieved with imatinib, at least in patients with adverse8 p0 U) m& I- \" t+ G: i6 I
disease features.
! h1 x' Y6 N* n& M |