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。/ v V5 A: d0 y' H2 C9 [ ~
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。7 [3 {2 v* V6 I1 z, u9 m
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作者：来自澳大利亚4 h5 R2 Q8 j1 w4 ~
来源：Haematologica. 2011.8.9.
0 L. I7 ~. V" i& P! V- @Dear Group,
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9 Z* v. b; o6 [: v- mSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML0 B+ \! ]/ E+ a* m3 J( L- @7 o
therapies. Here is a report from Australia on 3 patients who went off Sprycel$ T, f0 y9 e m, s3 P
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 S0 s# o; A. b$ Z0 o6 aremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel6 f1 M! H/ ?. X; P* g' x
does spike up the immune system so I hope more reports come out on this issue.
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. i7 l9 |8 Z3 E- uThe remarkable news about Sprycel cessation is that all 3 patients had failed
8 A. z9 L0 M2 P, u: |Gleevec and Sprycel was their second TKI so they had resistant disease. This is
; h, ]8 ?! W, `8 R/ ]0 u3 _% v/ cdifferent from the stopping Gleevec trial in France which only targets patients
4 U, w2 p; b) C2 U/ Swho have done well on Gleevec.1 c% G- L5 \5 Z
; t+ K& i5 w, k. DHopefully, the doctors will report on a larger study and long-term to see if the
& G# x+ ^9 u% y7 Z3 q9 T9 @. |response off Sprycel is sustained.6 \5 p8 D4 [3 C+ E/ `. i
) e7 P7 Y: ]% D1 l* l+ _ T3 DBest Wishes,: Z3 P. p; V& p0 p
Anjana
7 A& u& y3 A3 S: F* ]
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7 Y. i% @9 M+ h/ D
6 y; X B; q3 f+ [1 Q+ ?. h" D$ AHaematologica. 2011 Aug 9. [Epub ahead of print]
+ g. c, x4 {4 f/ s' J' b) ~8 fDurable complete molecular remission of chronic myeloid leukemia following5 H( i% W7 w- o
dasatinib cessation, despite adverse disease features./ @- s) f+ ~% s8 W7 Q) {, R
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.3 G) B2 s& L* n; C/ g* e7 } y
Source
; _* Z1 p+ z/ t9 n2 JAdelaide, Australia;
( {6 `/ E, i% i/ G2 V# q4 `3 Q9 h, S- {" K2 @; w7 c
Abstract. M$ f! R% p1 L7 a
Patients with chronic myeloid leukemia, treated with imatinib, who have a( X. V1 K9 i" g3 m) z" v$ B
durable complete molecular response might remain in CMR after stopping
; s' t( L) b& U' y- n% D* u4 jtreatment. Previous reports of patients stopping treatment in complete molecular
0 C; Z% T; W( presponse have included only patients with a good response to imatinib. We3 [' ^/ {) Z4 ]- {
describe three patients with stable complete molecular response on dasatinib; \8 \6 g; u" I- S/ l
treatment following imatinib failure. Two of the three patients remain in+ u0 n, o- @. h" l
complete molecular response more than 12 months after stopping dasatinib. In5 A1 I8 U* R% Z
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
4 I8 ?9 E1 ~6 j4 a Fshow that the leukemic clone remains detectable, as we have previously shown in, H! c' U) x' R( h
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
! j8 Y5 j# M# [+ B& R7 [& ithe emergence of clonal T cell populations, were observed both in one patient5 A/ C8 [) g0 m2 h& u, G* o
who relapsed and in one patient in remission. Our results suggest that the4 M& C7 a/ k1 a5 Z/ V7 i
characteristics of complete molecular response on dasatinib treatment may be
' q* j, h8 V! F" K6 _! nsimilar to that achieved with imatinib, at least in patients with adverse
# y: I9 Z% a6 @2 ^+ K; s+ h+ W! a9 kdisease features./ Y9 E1 ^5 f8 \2 C$ }. _9 G
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