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。
7 \, g% y6 d; c+ p 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。
4 ~+ E5 M% ?; A 2 C/ O/ `# J1 a. b# w4 G2 i) |: O
作者：来自澳大利亚
% ~3 G6 w) X5 Q( g! [来源：Haematologica. 2011.8.9.
p6 ^' S5 E7 F! F, ?, IDear Group,6 W4 |9 Q: i/ E+ p) W
! @1 D: i: @) g5 v1 a8 X# j4 V, iSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML, j, U& X" ]/ P, N8 v& o9 e+ p
therapies. Here is a report from Australia on 3 patients who went off Sprycel
2 p! v0 `6 r' Y1 Y* zafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients* i2 u2 v4 V0 v
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- i9 F( {# ~5 fdoes spike up the immune system so I hope more reports come out on this issue.
- T% [2 |; Y+ h6 @- ^1 w+ t2 L# ?% H2 }5 S6 t7 P% m% n3 M
The remarkable news about Sprycel cessation is that all 3 patients had failed( i+ B6 g/ O8 o: z
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
+ G( l: j' Y, v# U3 Q( e1 ldifferent from the stopping Gleevec trial in France which only targets patients( K6 E1 Z+ _4 ^5 C2 V+ J6 m/ P
who have done well on Gleevec.
7 W% g3 ]2 U& i1 z0 H# s. A) D, ^8 z% R
) p, u7 W# L ~6 X! C! GHopefully, the doctors will report on a larger study and long-term to see if the
8 d0 D3 n2 r1 Fresponse off Sprycel is sustained.5 m2 E( q( q9 f2 S+ u9 u; P3 V6 t
3 r3 R* {8 }( R" c6 N# X7 D0 Q- g1 @Best Wishes,' u. X5 ?5 x- A& d8 S) ^4 ]' |. t& Q
Anjana
% K' B" Y6 u6 I2 ~0 K3 J8 _
/ b) X$ B" c, }* [% w) H- V" A J; q7 B D2 r, _! Q
p( W) J9 }2 S. {7 k @Haematologica. 2011 Aug 9. [Epub ahead of print]
* x- N" M, u6 c0 wDurable complete molecular remission of chronic myeloid leukemia following- f( A, Q6 e( U
dasatinib cessation, despite adverse disease features.
; o3 \* ]2 c& b/ z1 RRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.7 }4 X& o& }6 S. i; t1 ?! x$ H0 ?
Source
8 K s$ w+ Z: i! U6 x4 b: rAdelaide, Australia;
, p l) A& s7 C& R/ G6 k# Z1 ~, H' d }, W. m3 h' }* Q$ }9 _6 S- U
Abstract
) _4 l. M' j! z0 H4 E. T5 kPatients with chronic myeloid leukemia, treated with imatinib, who have a
' H2 y6 O% W) ^# Ydurable complete molecular response might remain in CMR after stopping
9 w; p* W) V ? @treatment. Previous reports of patients stopping treatment in complete molecular; {. Y/ z( }7 `
response have included only patients with a good response to imatinib. We' A; t. G, \! @; O. z" j
describe three patients with stable complete molecular response on dasatinib+ V; {' W* [5 b, ]. r
treatment following imatinib failure. Two of the three patients remain in" H/ r @4 u& _7 H# l
complete molecular response more than 12 months after stopping dasatinib. In1 D d1 Z4 Q4 y; ?7 A
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
8 N; w1 o0 \! P% oshow that the leukemic clone remains detectable, as we have previously shown in# n5 r3 r! Z4 ^7 Q7 G+ G
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
! u3 n- s" E( r) B# X3 H8 ]the emergence of clonal T cell populations, were observed both in one patient
! t4 s8 K/ U% _, ~; N" ^who relapsed and in one patient in remission. Our results suggest that the
0 b( ^' l- P0 V9 gcharacteristics of complete molecular response on dasatinib treatment may be. A; E8 C# h; ^/ G% B0 F' L7 P0 H
similar to that achieved with imatinib, at least in patients with adverse; @4 g/ d8 p- _" g- n
disease features.2 y7 W3 ^8 _- w: [2 x6 o
|
显身卡
