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。0 B4 A6 l) R" |- d: y3 ^
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。2 Q+ F7 C' w% d- o8 h. T
3 X; b7 A1 A1 a5 @; h* `作者:来自澳大利亚, G, P3 M) M' A. y, A4 C& G
来源:Haematologica. 2011.8.9.
3 D) w( ~, F& z5 Y& u! mDear Group,
3 i8 |8 ~% H- L# |1 s/ I
5 M: M* M% ?. H8 e/ p% z3 pSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
" S, r$ W' R- Z9 rtherapies. Here is a report from Australia on 3 patients who went off Sprycel
* L" t% V4 }0 b" wafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients4 l! y% B) a' Y9 q y ]
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
. r6 m6 E: Y' wdoes spike up the immune system so I hope more reports come out on this issue. `, A0 I2 w0 \. R2 d! N5 k2 M
, e. y( J) q5 B5 J& R2 H* j4 oThe remarkable news about Sprycel cessation is that all 3 patients had failed3 [- D0 B$ a5 \8 v$ O
Gleevec and Sprycel was their second TKI so they had resistant disease. This is I4 j D* D) ?5 }3 Q' H" B" `
different from the stopping Gleevec trial in France which only targets patients
" V P+ k8 Z: w/ L4 f1 M: zwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
' F; E- [5 S; @6 l/ nresponse off Sprycel is sustained.
3 o+ L- n( {# h' R# \
0 b; ]. \! Z% K8 w! rBest Wishes,
7 U& d4 c6 C# l3 v3 M" ~) hAnjana; f9 I0 F1 W6 }2 @1 r4 {' e
x' s: S& w4 I4 x
3 d! m' f( k1 v/ |
: g! F! r8 s% C; g9 \Haematologica. 2011 Aug 9. [Epub ahead of print]
: _! e t5 I1 Y* c, q* KDurable complete molecular remission of chronic myeloid leukemia following7 @8 _) l% Z3 f- f
dasatinib cessation, despite adverse disease features.
# W) f) }7 u3 x1 \; G. q" U; jRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
/ @! T0 r/ K* P( u, Q0 ^Source
- Y/ B) Q( ^$ M0 `- DAdelaide, Australia;8 w5 R. s( N3 [$ W5 ~ j
3 |0 {) b0 ?. k" S; D4 u/ \
Abstract
3 b) {: z+ E9 Q) Z$ y5 yPatients with chronic myeloid leukemia, treated with imatinib, who have a
3 z8 U& f% D0 N; r, s% w) ydurable complete molecular response might remain in CMR after stopping
Y1 m( N) a8 |( t, utreatment. Previous reports of patients stopping treatment in complete molecular( J, L. N- `' O. J
response have included only patients with a good response to imatinib. We1 |* ^6 s f+ {8 K
describe three patients with stable complete molecular response on dasatinib
' k- w2 M" s- w5 mtreatment following imatinib failure. Two of the three patients remain in; q: C4 u) K* E* X0 r
complete molecular response more than 12 months after stopping dasatinib. In4 `) Q! U& \% T% W
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to! |+ I% ]) t4 f
show that the leukemic clone remains detectable, as we have previously shown in
! Q4 h1 n& P3 h) }2 Z5 A6 rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 j3 L/ Y) Q& e% V) j0 B) Wthe emergence of clonal T cell populations, were observed both in one patient
5 F: `! I, ~$ J* p0 ^7 m! P; [- awho relapsed and in one patient in remission. Our results suggest that the2 z) H }9 ]" x$ a' v7 b R& o
characteristics of complete molecular response on dasatinib treatment may be; i' d. E+ s/ l, @- N7 [' f; g
similar to that achieved with imatinib, at least in patients with adverse
5 L( r. X" j; \; Q6 `disease features.
) B1 E, |% Z* E* k) f# Y w |