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。
3 J8 ^7 D; P. Z6 l" c; W1 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。
7 h1 X, E8 V6 ^, \- E 6 I0 n9 F( q( ?/ m" S, h2 a- }2 T
作者:来自澳大利亚4 P! w2 n9 E7 t0 Y1 N
来源:Haematologica. 2011.8.9.( K! q. i6 n2 P/ I7 \3 Q
Dear Group,5 o7 |1 @2 w5 L( [! y" T" h
. \" V. H% U/ \
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: g9 m K( P. Jtherapies. Here is a report from Australia on 3 patients who went off Sprycel5 w0 E) Q& s* v7 j
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
: Y' T/ ^( c4 j3 `' Z9 y! Y: Zremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
2 ]5 `: z( t3 } [5 ]1 Ndoes spike up the immune system so I hope more reports come out on this issue.3 d7 P9 ^% E4 i9 p
2 o- P5 a6 b! G( x8 m' DThe remarkable news about Sprycel cessation is that all 3 patients had failed5 J; h/ P5 z: R* l
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
( `1 f2 Q3 n1 {$ t# \7 Mdifferent from the stopping Gleevec trial in France which only targets patients- l# j4 J4 Q/ O1 j3 c; M* A
who have done well on Gleevec.' B( W6 O4 x# D0 P( K4 W
/ t m" e# e- J- O: C1 h5 MHopefully, the doctors will report on a larger study and long-term to see if the) A& r# q2 s2 }$ O7 l, p
response off Sprycel is sustained.* Y* v8 Y/ Z. S/ ^4 y
0 G! D8 l- Q! Q3 |
Best Wishes, M# }( F; Z3 b; R, B% Z. N. h
Anjana- q. Q& L1 }5 h" C8 ^
, @2 U3 X- d' o8 t1 ^) X
2 C# Z' t" ~6 u, w4 L4 }; B2 h. V
8 k- i) G }! w# h$ k' m
Haematologica. 2011 Aug 9. [Epub ahead of print]
: _1 ^( z1 |5 @8 F C$ q; rDurable complete molecular remission of chronic myeloid leukemia following
- m3 ]! i! x, T. odasatinib cessation, despite adverse disease features.
1 Y2 Y$ [- I g) z8 CRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
" X) B. F3 C, ]. o0 @0 p5 l# B8 F& _Source
6 T7 K8 D- S8 O' b1 z# h. vAdelaide, Australia;
9 G3 k1 n. J9 l6 n( s& _4 J- _
: X1 Q& f: y# r( ?- A, [Abstract
; E! o9 s0 X/ b1 e5 H- O) FPatients with chronic myeloid leukemia, treated with imatinib, who have a7 S4 _4 g& L6 e& i& G, I" }) [
durable complete molecular response might remain in CMR after stopping/ E: z4 q( a( p$ u0 S' u8 ^
treatment. Previous reports of patients stopping treatment in complete molecular
: k" e7 y S% f# o2 Lresponse have included only patients with a good response to imatinib. We. M% U9 |0 S& S
describe three patients with stable complete molecular response on dasatinib
/ E5 O' O" P) y1 wtreatment following imatinib failure. Two of the three patients remain in5 _" {# u5 |5 k1 N3 O& j4 S
complete molecular response more than 12 months after stopping dasatinib. In( ^" x' b, [: y+ R9 K! v; y- H. A
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to8 s, K4 U; M3 Y9 G
show that the leukemic clone remains detectable, as we have previously shown in
+ |& Q, u) a1 U4 h" I6 U) X& y6 Eimatinib-treated patients. Dasatinib-associated immunological phenomena, such as; D# B: o# o/ |7 l! @& r/ F
the emergence of clonal T cell populations, were observed both in one patient
3 `# K9 q5 M- j! b/ t5 ]$ }( vwho relapsed and in one patient in remission. Our results suggest that the
% x3 F3 ]) X! M- [characteristics of complete molecular response on dasatinib treatment may be
7 U% s! B5 S$ s6 \! i; i* w/ J3 tsimilar to that achieved with imatinib, at least in patients with adverse' \" |% N G* K% f( T" n
disease features.
2 {6 N1 Q% Q B1 | |