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。
L9 C( }1 h3 D4 M& }: ? 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。& T. S% ]9 e' T8 I0 n
: X% U1 ^+ [7 t9 C: g- u; N' N作者:来自澳大利亚
) ^4 K' M3 Q5 D来源:Haematologica. 2011.8.9.: T. E! X6 s) x4 d* I% c- D" M
Dear Group,- u' h( v8 g+ V) Y" W
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
( d. Z5 {0 U7 O n# A- Q6 D ^" ytherapies. Here is a report from Australia on 3 patients who went off Sprycel
- o+ H9 ^' K9 D5 L5 rafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 J* b; B3 H: u, v gremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel, M5 z; z7 C D$ O$ {% }( y
does spike up the immune system so I hope more reports come out on this issue.
( J. C+ O+ L; @: A X+ p1 B5 B- P, Q, G& e$ a
The remarkable news about Sprycel cessation is that all 3 patients had failed# i! B- S+ | W! a0 S
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
* [: p3 A6 Q4 v( \+ Z8 Y3 k- Kdifferent from the stopping Gleevec trial in France which only targets patients! Q; ^; C6 ?- p7 D
who have done well on Gleevec., \+ k5 V4 q- B* s' p5 g
1 Q. Q1 T$ k% E
Hopefully, the doctors will report on a larger study and long-term to see if the
1 Q# ]& g& ~; F9 u% [response off Sprycel is sustained.
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Best Wishes,3 j$ ^ N/ n# n4 @ d: U1 Z
Anjana8 ~$ H. [2 h# h4 y2 l$ \& j4 Z
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Haematologica. 2011 Aug 9. [Epub ahead of print]6 f( H& c7 p- S% o/ D5 |- C8 T+ g
Durable complete molecular remission of chronic myeloid leukemia following
' y* ?( R# O0 p! E* R3 X, M" @- Ddasatinib cessation, despite adverse disease features.
( s! R' g$ H# W6 t" _1 W& |4 ?Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
2 M+ {- ^0 o* |* U' hSource
. }. |2 z- a+ B5 YAdelaide, Australia;
6 B) B3 U, {* l8 @2 S7 x2 D8 g$ ]
Abstract; l9 W+ S" @8 Z: {" [; g# _
Patients with chronic myeloid leukemia, treated with imatinib, who have a) D5 T; r, c/ Y$ x% {( B
durable complete molecular response might remain in CMR after stopping6 m* F& ?" E$ s7 }5 ^$ n6 M/ z' C
treatment. Previous reports of patients stopping treatment in complete molecular
" L; e9 _% a. @- G) zresponse have included only patients with a good response to imatinib. We
( z# q; g/ b% L' B9 a0 qdescribe three patients with stable complete molecular response on dasatinib% N$ N. ~+ N& K! y# x! z' t0 o
treatment following imatinib failure. Two of the three patients remain in
- H3 }: j) K, E; X3 W8 K0 ncomplete molecular response more than 12 months after stopping dasatinib. In
. y. f8 B+ m* z5 D( Y5 ~these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to$ T/ b9 d" T$ Q$ H, v
show that the leukemic clone remains detectable, as we have previously shown in
1 D0 M- N" d$ E; Qimatinib-treated patients. Dasatinib-associated immunological phenomena, such as1 s& n2 `; p) P
the emergence of clonal T cell populations, were observed both in one patient6 m& a$ ?6 T4 c
who relapsed and in one patient in remission. Our results suggest that the
o# m+ F' m+ e7 u4 ?characteristics of complete molecular response on dasatinib treatment may be
0 S1 [( m7 r, Isimilar to that achieved with imatinib, at least in patients with adverse% `4 S; W8 j; e* d4 ]/ H' h) S
disease features.
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