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。% v; c6 e. o( d+ b( [& 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。. }8 x m0 |8 Z- ~9 A$ Y6 K
) }8 g r/ A) h/ K作者:来自澳大利亚
! e9 B6 C* z( `( X! g来源:Haematologica. 2011.8.9.
1 r8 N5 A4 E M9 m( `$ N+ q" QDear Group,' j, ]5 b/ H- o$ r
& q, E$ a; ^4 e8 J7 a" N0 zSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML2 D' i1 H9 O E% |
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 y& f7 p. ^7 R3 t
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients8 \$ ]: `' D' Z0 G+ l- K9 P
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( U& X1 f* |9 J4 L1 o- C2 ]
does spike up the immune system so I hope more reports come out on this issue.7 ^5 H7 E8 `! ~3 j' X) P% \
8 V" f& Q* d. f+ U: b* t
The remarkable news about Sprycel cessation is that all 3 patients had failed, B3 Y$ L6 z) J# b& @3 Y: h
Gleevec and Sprycel was their second TKI so they had resistant disease. This is1 s4 e+ _5 j- k2 C9 l; Y
different from the stopping Gleevec trial in France which only targets patients* }& e! z! c( m4 p
who have done well on Gleevec.- Z' R4 |7 p1 P
* k6 S1 } T* _# W$ k% p7 G# QHopefully, the doctors will report on a larger study and long-term to see if the( S2 d/ C9 y2 H3 ^: U
response off Sprycel is sustained.
& ~4 y( U9 F2 q: Q& F" {7 h8 ]+ S# B$ W
Best Wishes,
5 n4 J6 U. s% C! k- \Anjana
. k0 L7 q, W9 ]; y+ _ ]
- ]) \+ a3 A% i7 e$ h9 [
1 T/ A3 d3 T$ q
/ E" c' S0 k; A% \$ AHaematologica. 2011 Aug 9. [Epub ahead of print]
6 J: _0 ^7 W% z2 ^% m$ RDurable complete molecular remission of chronic myeloid leukemia following
4 a$ I7 y' F* B) W" Qdasatinib cessation, despite adverse disease features.; t' W. I* s9 _( u( ^: j
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ O0 ]# f8 `1 [' k$ x7 H' B
Source
/ l1 d. \, j" l5 W' U/ `: g: i8 DAdelaide, Australia;
+ D1 E" V& x. |9 z/ G0 b2 Q5 Y( ?. I3 p5 w
Abstract
9 ^& T) W s) kPatients with chronic myeloid leukemia, treated with imatinib, who have a: @' g& [4 W' y6 [
durable complete molecular response might remain in CMR after stopping( Z! y7 N1 x1 z; g% ?( A
treatment. Previous reports of patients stopping treatment in complete molecular/ B& Q0 Y% t/ l K( M
response have included only patients with a good response to imatinib. We
- i( g- Z! i& G: q6 A. C& r+ Gdescribe three patients with stable complete molecular response on dasatinib) c0 m: f4 E/ c$ y0 S0 J/ K
treatment following imatinib failure. Two of the three patients remain in
g0 S) a# H& Xcomplete molecular response more than 12 months after stopping dasatinib. In- @, [* d! a7 r
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
: v. V# F% W- V2 [2 m w3 j1 Ashow that the leukemic clone remains detectable, as we have previously shown in
( R1 Q, S' E n% f/ {9 `imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
! X+ y+ ~7 O/ S7 V# Bthe emergence of clonal T cell populations, were observed both in one patient
( M2 t( u: a. \) @. k" Fwho relapsed and in one patient in remission. Our results suggest that the0 \( F/ p/ C/ a6 B6 w* i
characteristics of complete molecular response on dasatinib treatment may be
/ R8 U3 L, {3 U% _+ Y, t- \4 |. fsimilar to that achieved with imatinib, at least in patients with adverse
- L: M4 G# k% Rdisease features.
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