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 h4 I+ g9 p, R' Y 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。( K5 x- M# }- G9 Y
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作者:来自澳大利亚
4 b$ {4 a/ w4 `' S" L0 B2 J' Z来源:Haematologica. 2011.8.9.5 h% K! }0 U. N6 O+ Y
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
/ J4 Z, ^% |# X/ htherapies. Here is a report from Australia on 3 patients who went off Sprycel
8 S5 H2 h( N1 Gafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients- K9 K: x/ T' u/ V/ s
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel" N6 m* y8 U+ L b) Z; ]6 T" Q7 `
does spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed
3 F0 i0 N4 T: q- h" J/ |0 p8 x/ UGleevec and Sprycel was their second TKI so they had resistant disease. This is; z! h% N0 r$ p- Z7 T6 q [- M3 h
different from the stopping Gleevec trial in France which only targets patients
$ F% T3 L# h/ t5 I% @8 ~! }( kwho 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
1 a( _9 w# c+ S- H+ Yresponse off Sprycel is sustained.; q- V# S9 b# }& t$ q# \
: M7 ^4 ^+ o/ w; M6 E$ vBest Wishes,
- U, w0 H. ]0 p9 E+ c y; T1 hAnjana. L$ W z& q* f- B3 p5 S2 x
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Haematologica. 2011 Aug 9. [Epub ahead of print]
* D! x, H+ |8 K+ k, p) L/ }Durable complete molecular remission of chronic myeloid leukemia following- I! J0 Y6 A$ P2 c1 n0 ?
dasatinib cessation, despite adverse disease features.
5 f( R/ z$ W+ ]* FRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.0 i8 g# c9 O: p. n
Source
' V7 A1 ]8 \2 e% d" V* q+ TAdelaide, Australia;; A7 Y8 {$ A3 O8 L( O, @' V
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Abstract
$ |; O% R6 [8 d. I8 ~Patients with chronic myeloid leukemia, treated with imatinib, who have a
5 b- s: u" q& ^8 K& @, Ydurable complete molecular response might remain in CMR after stopping6 f1 n% |) m ?9 B' ~8 S
treatment. Previous reports of patients stopping treatment in complete molecular
% A* J% V, j8 C6 Y( gresponse have included only patients with a good response to imatinib. We
6 k% E# d% L) x2 ydescribe three patients with stable complete molecular response on dasatinib
) g* `+ Z: k& n' A, a& y dtreatment following imatinib failure. Two of the three patients remain in& T+ R7 r& e7 r# Y+ L5 }
complete molecular response more than 12 months after stopping dasatinib. In
* J1 E+ N8 |2 N s8 pthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to" Q' X% ^9 c% I- L! b
show that the leukemic clone remains detectable, as we have previously shown in
6 T W2 a/ B' I5 p' a, R7 wimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
4 [; a1 h+ x' A6 B% u/ ?the emergence of clonal T cell populations, were observed both in one patient% T9 O7 |- v# p5 ~$ w" K
who relapsed and in one patient in remission. Our results suggest that the
4 V4 J. p7 _2 @# \ W/ g( s( Rcharacteristics of complete molecular response on dasatinib treatment may be: g. S- t5 P" C; I. P: e8 j* @
similar to that achieved with imatinib, at least in patients with adverse( v+ V# s0 v3 ^+ [& b$ `. z
disease features.9 |% ^. }0 W; A ?$ ~7 X, ?- e! Y
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