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。( ?! \* U* o) ]0 s- }4 I& i% ]
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。- g3 ~6 {/ [4 z) C- f1 S1 }( \0 ?
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作者：来自澳大利亚
# w6 ^4 r- {! U" a5 }2 ~: |. N: w来源：Haematologica. 2011.8.9.
) T0 \9 p, G2 @+ iDear Group,
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9 L% d( z; _" a, p) u6 R. S% N- m- QSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML) N7 i) G% q0 H4 R% j# ` [* v1 \% Z
therapies. Here is a report from Australia on 3 patients who went off Sprycel
8 e. V" i) ]$ Oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
4 {( T* Z; ^: m H; }remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel4 ]; k* X9 r6 p/ H/ l
does spike up the immune system so I hope more reports come out on this issue.* y: t" F N; x: t n5 X, A7 b- y
6 N) ]/ ~( D$ i+ Z! c3 oThe remarkable news about Sprycel cessation is that all 3 patients had failed
4 y; M; w: w/ m- z; S; g1 L, dGleevec and Sprycel was their second TKI so they had resistant disease. This is
$ n7 l1 f# f2 p) G% m( F& Q2 Ydifferent from the stopping Gleevec trial in France which only targets patients
; G: e# e+ L* B+ V8 X* C/ C3 fwho have done well on Gleevec.! Z/ t/ R; u( _8 l# K6 {" l4 k
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Hopefully, the doctors will report on a larger study and long-term to see if the
) y, t0 _) } T) w' W0 aresponse off Sprycel is sustained.
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Best Wishes," S; {5 p" [9 v
Anjana8 d$ L8 \" V9 h
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Haematologica. 2011 Aug 9. [Epub ahead of print]
g/ U0 e, N' C+ m, U8 [+ f0 E# ~% vDurable complete molecular remission of chronic myeloid leukemia following7 N. e0 d+ L- y" r# R+ m
dasatinib cessation, despite adverse disease features.4 m5 o/ M" L! n% z6 F( z
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;
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Abstract5 s/ c- m1 R- m: m( P5 I
Patients with chronic myeloid leukemia, treated with imatinib, who have a
8 d9 e9 _" C0 ^durable complete molecular response might remain in CMR after stopping p6 z' T! {$ e
treatment. Previous reports of patients stopping treatment in complete molecular& F/ B# x& \3 u# p
response have included only patients with a good response to imatinib. We. Z- N. x" d- Y0 \* X- y( r y
describe three patients with stable complete molecular response on dasatinib
! K& ^: T6 q# P, s' S) jtreatment following imatinib failure. Two of the three patients remain in. q3 ~. r' O6 w% K: O$ m
complete molecular response more than 12 months after stopping dasatinib. In' T3 R) p4 q3 X @9 U: R
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to* H: Y' H9 i9 v \
show that the leukemic clone remains detectable, as we have previously shown in/ K6 ?6 m! @9 ~9 o9 z3 H* K
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as6 V! r: Y( e3 K5 \
the emergence of clonal T cell populations, were observed both in one patient
; E/ \3 [! F" h, a6 `' `who relapsed and in one patient in remission. Our results suggest that the
* h# e+ J7 u+ ^8 G9 mcharacteristics of complete molecular response on dasatinib treatment may be7 b* A5 `% x- ?* C2 [
similar to that achieved with imatinib, at least in patients with adverse
, D2 U" L9 W2 U, _$ |% Vdisease features.
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