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。. W8 X H$ @" k" O
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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作者:来自澳大利亚
/ r2 G- X R c1 E. ~* Y来源:Haematologica. 2011.8.9.
% Y _" Y) ]' I8 e* X/ _; qDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML9 C0 U! b$ {9 F3 R' j
therapies. Here is a report from Australia on 3 patients who went off Sprycel2 ]& e+ I7 a2 m7 K7 }1 P7 P: O
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
( B* {' P8 A' T( G5 jremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. {, \5 _1 j4 u
does spike up the immune system so I hope more reports come out on this issue.
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- ~% V7 O0 F4 S6 G5 ]) WThe remarkable news about Sprycel cessation is that all 3 patients had failed5 P8 v( Y- z* k- u) z
Gleevec and Sprycel was their second TKI so they had resistant disease. This is& V' x; r# z; s g: p
different from the stopping Gleevec trial in France which only targets patients
1 x1 C) n8 T( g9 G# Bwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the4 B2 u u7 x! }+ I
response off Sprycel is sustained.6 s- i( D9 J5 \# R6 T6 x0 A
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Best Wishes,
5 Z( `, I1 |7 y0 L8 {Anjana
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5 C5 F: U2 `% w$ oHaematologica. 2011 Aug 9. [Epub ahead of print], J, y- l i( C$ q. E, _
Durable complete molecular remission of chronic myeloid leukemia following; a9 g& V4 o2 e: j0 U2 k/ {3 B, R
dasatinib cessation, despite adverse disease features.
$ T; B8 E* ]. f$ k4 @/ IRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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3 X: n4 U) i; l* o5 H8 Z, v2 t1 m/ DAdelaide, Australia;% A/ T3 q0 N V2 m. u0 Z) h
" W, g t3 C' i6 ]Abstract8 T$ a1 u1 o" }( A0 N
Patients with chronic myeloid leukemia, treated with imatinib, who have a4 H& z3 Q2 \" X8 q% C
durable complete molecular response might remain in CMR after stopping
2 n$ R" D) E6 w- xtreatment. Previous reports of patients stopping treatment in complete molecular
7 H8 R3 @3 H \/ p* Fresponse have included only patients with a good response to imatinib. We
. {) g5 m% K1 t' T$ @describe three patients with stable complete molecular response on dasatinib
1 j* U4 g" |+ Z8 ?8 ^8 w7 U& B0 jtreatment following imatinib failure. Two of the three patients remain in8 n: O, }, d0 q$ }$ Y
complete molecular response more than 12 months after stopping dasatinib. In
; a B# P/ l) p! m) M# K1 Dthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
! {# |! L, w# g, p4 oshow that the leukemic clone remains detectable, as we have previously shown in
, l% E* {4 U0 A3 Z1 s8 \4 _; oimatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 ~ e/ }0 I, |; O, o _, ?7 ]3 L
the emergence of clonal T cell populations, were observed both in one patient- a3 T% K2 r3 j
who relapsed and in one patient in remission. Our results suggest that the
( Y; i& [& G/ ~% ~characteristics of complete molecular response on dasatinib treatment may be: B' l' {! O8 C. ^
similar to that achieved with imatinib, at least in patients with adverse
: G. a1 \3 e9 s; b4 q" P$ `& Zdisease features.' J3 y# |5 V: V) E# D1 B
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