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。 q2 Y* ^9 W8 F
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。/ g/ U! M |3 _
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作者:来自澳大利亚+ `1 ?( u* y! n: M# |
来源:Haematologica. 2011.8.9.
0 t8 s7 q, T0 Q" L* E6 p, f* E7 j5 RDear Group,
0 h8 z5 q7 F. _( i& a6 x
8 ]! i) t2 U% Q+ Y4 ZSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
4 \& P* ~( j6 ftherapies. Here is a report from Australia on 3 patients who went off Sprycel& i' @1 `8 K2 i- Q: H& Q8 m7 \
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients( ]3 ?7 p; E* ~' c4 h8 B
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' L- n2 y: {8 g U, G4 S, ~
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, u3 Z" a2 A* f7 V
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
( v" `! Y/ `) l; n7 P, n# Udifferent from the stopping Gleevec trial in France which only targets patients
3 p1 V( ] a) \- U; _who have done well on Gleevec.
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' P5 s7 b4 |( xHopefully, the doctors will report on a larger study and long-term to see if the! C- j" A& ?) d- s& v! V' i k" |
response off Sprycel is sustained.& f. R8 u7 q- }; b5 M
; G z+ P. l; M& P2 F" VBest Wishes,
+ e0 y, m+ N5 i* k7 wAnjana
: @ C, m( r) ^. X+ P) e9 S! b- p( d+ _3 u( P9 _- R6 D F {
/ G4 `8 h3 I- N" V7 r5 q% u0 { ]
; E+ ]- r5 G6 P0 oHaematologica. 2011 Aug 9. [Epub ahead of print]
9 C6 }+ N r9 T) C% `1 j f U* yDurable complete molecular remission of chronic myeloid leukemia following9 L" e% o2 S s/ [8 L
dasatinib cessation, despite adverse disease features.4 n; R7 G8 ?: A4 ?9 q
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ C1 Q9 D4 A5 V) Q0 P4 w) t/ Z
Source
) |' a; i# W) @+ Z; n: P( h4 mAdelaide, Australia;
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s1 C+ ^; x; \% z3 w$ lAbstract
) e u6 e0 V: X/ T# E4 kPatients with chronic myeloid leukemia, treated with imatinib, who have a# M. k7 d8 ?* G% y2 w
durable complete molecular response might remain in CMR after stopping
' o1 { D, M }( O+ rtreatment. Previous reports of patients stopping treatment in complete molecular5 W n+ B( ^' N! G* m8 P ?( o
response have included only patients with a good response to imatinib. We
5 X0 N0 j( R# P' Jdescribe three patients with stable complete molecular response on dasatinib
& L# P2 @. @$ @) |% h5 ytreatment following imatinib failure. Two of the three patients remain in
" \8 ?( f' W: w# Zcomplete molecular response more than 12 months after stopping dasatinib. In
# r, y' I0 U+ W/ A0 M8 p' |: Wthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
. \+ E& o! R/ c0 y" r9 \4 v1 k& ^show that the leukemic clone remains detectable, as we have previously shown in* m5 P7 I% k; i, L. u5 k; W% W
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ v) s6 d: C% \0 {the emergence of clonal T cell populations, were observed both in one patient
# E. W2 n, }2 |( f8 y5 C9 Xwho relapsed and in one patient in remission. Our results suggest that the4 B* L, M! F/ N; J
characteristics of complete molecular response on dasatinib treatment may be
( Q% u; _6 t b) J$ Rsimilar to that achieved with imatinib, at least in patients with adverse
3 O F6 B2 k+ Bdisease features.
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