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。
, U7 L% q3 H1 C+ f4 A S/ \ 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。
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6 y6 E/ a& k3 p) Z# ~6 c4 U作者:来自澳大利亚6 x- K# J' f4 }4 R& e6 a* r# X
来源:Haematologica. 2011.8.9.
1 m. {: k; [" @6 g6 z6 Y( b! i, aDear Group,( A0 t- o! T% K2 y3 L
3 s7 l- \+ C# v* d3 h+ tSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ [1 Z1 t2 C( N+ D# l
therapies. Here is a report from Australia on 3 patients who went off Sprycel7 U0 c9 I* k; c3 e6 U
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
y4 M5 P. X% Vremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel$ l# ^2 k% { w6 A1 J ]# I- G
does spike up the immune system so I hope more reports come out on this issue.# _5 H- y+ \. v# g' @
2 \; @) T- j a& i+ ~2 ?/ AThe remarkable news about Sprycel cessation is that all 3 patients had failed
- K/ h# z0 k/ s: P& o8 S* _/ rGleevec and Sprycel was their second TKI so they had resistant disease. This is
& e9 r* c" ~5 S# e0 ^- G2 Adifferent from the stopping Gleevec trial in France which only targets patients
: P2 Z6 E9 z S+ M! vwho have done well on Gleevec.
5 s7 A/ X' B- _) Y& S+ X% P! W4 i9 F3 O3 [$ O( p. D W, M& r1 e
Hopefully, the doctors will report on a larger study and long-term to see if the
0 ?4 S/ w T5 sresponse off Sprycel is sustained.8 `! r7 N7 F( r* Y: _1 O/ M
; v4 @5 y. c6 \: J. g7 B- NBest Wishes,& o3 W4 _: ?: @* B" H
Anjana5 X1 ~7 f: L+ @( t
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Haematologica. 2011 Aug 9. [Epub ahead of print]
# n5 l' }! b6 ?& S* H2 l9 q2 DDurable complete molecular remission of chronic myeloid leukemia following1 {, z+ f5 y3 J% m; y
dasatinib cessation, despite adverse disease features." P- c$ l- g# p+ k! V/ h
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
4 d, ~* R" P0 J) x) v, b2 \Source
2 {7 n' _6 ~* a: O! U: h9 R, a' KAdelaide, Australia;! M' ?2 f7 ~7 V
6 d8 ~* `: D$ p4 E! |" \; S a: d
Abstract' g- [) y0 p# L' D, l+ W
Patients with chronic myeloid leukemia, treated with imatinib, who have a
6 F! d5 c5 _; D8 P1 X& ]durable complete molecular response might remain in CMR after stopping
; Y4 g' h+ Z4 a; ?! V2 x* mtreatment. Previous reports of patients stopping treatment in complete molecular
* Y0 o$ ^2 [9 L7 Bresponse have included only patients with a good response to imatinib. We
- b5 h K5 t7 U% q$ N9 [! G0 }0 `describe three patients with stable complete molecular response on dasatinib) {3 g" T& ^% N1 _5 @& J( x; l
treatment following imatinib failure. Two of the three patients remain in
2 j4 G/ d' N/ _* x5 r" [, ~ f+ Qcomplete molecular response more than 12 months after stopping dasatinib. In p" m. g( Q3 P; X5 K
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
3 W1 P8 L$ O6 `- J" bshow that the leukemic clone remains detectable, as we have previously shown in$ v" n0 W/ W) n
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
) l$ u% X9 j, f2 J, l) c. q' Ythe emergence of clonal T cell populations, were observed both in one patient
( \2 x' y( z) x* ^who relapsed and in one patient in remission. Our results suggest that the
! ?$ R; N' o! G7 m) b9 K( }characteristics of complete molecular response on dasatinib treatment may be
+ v# X4 z y9 y \& qsimilar to that achieved with imatinib, at least in patients with adverse
( S% J4 I. r6 _* \* p* sdisease features.% r1 ?( }% `7 | n" ~" {1 p" H
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