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。
; P# C, C% Z; G1 z, ]: g 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
% v" s: K- B* A$ X) ]2 w1 H$ H% Q来源:Haematologica. 2011.8.9.
6 e. R9 p0 K9 HDear Group,3 v( Y$ D/ {" Z9 e+ D/ ^
: j( ~( e2 q" W% vSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
+ k! L6 S# s+ |5 ?8 d9 Ctherapies. Here is a report from Australia on 3 patients who went off Sprycel
; q% s5 K! b0 L' F: Wafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients% M# s; ^0 z7 p; b) q$ D
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel: P3 c) j4 a `* Q- ^# J
does spike up the immune system so I hope more reports come out on this issue.
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% n" x2 o5 }0 UThe remarkable news about Sprycel cessation is that all 3 patients had failed+ [4 I) X* j+ ]6 C* O! r
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
5 _2 H9 [% \, j. T& [different from the stopping Gleevec trial in France which only targets patients; \7 x/ V4 ?- P- J) J7 X: P9 a
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
0 S' M" X$ g% H7 ?9 g! ~response off Sprycel is sustained.
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Best Wishes,
M* S+ [- Y& ?/ d' G, C, GAnjana
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0 B; H# {5 i% d( J( d/ cHaematologica. 2011 Aug 9. [Epub ahead of print]) r# @4 |( q4 }: v% J d( R0 X
Durable complete molecular remission of chronic myeloid leukemia following
8 w2 @. |7 g4 F z5 ~# z; K3 o4 tdasatinib cessation, despite adverse disease features.
7 J1 }& c" n" a6 w5 f/ yRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
" L- A! _+ V$ g$ A: ]0 uSource
. ^/ j' e6 V& Z* S' dAdelaide, Australia;
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( [' c+ o2 r( B2 q: E: T& k+ sAbstract
/ r2 D- B# x' m+ E& J+ S+ L! APatients with chronic myeloid leukemia, treated with imatinib, who have a
. O4 G' R" {, f; F6 t* D+ T4 ]durable complete molecular response might remain in CMR after stopping
, D9 B9 o9 }' ]$ M! Ktreatment. Previous reports of patients stopping treatment in complete molecular
8 S6 Y- H' |1 x1 r0 cresponse have included only patients with a good response to imatinib. We
5 ~2 h. N4 B$ L/ w, U$ \describe three patients with stable complete molecular response on dasatinib
' d Q( o7 h0 y& ptreatment following imatinib failure. Two of the three patients remain in% ^, r! g# |$ k0 y9 k% x# v
complete molecular response more than 12 months after stopping dasatinib. In
5 Y* m: C: t" |7 \8 ]! Sthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
; y, U5 E8 ~! a1 T) ?; H0 bshow that the leukemic clone remains detectable, as we have previously shown in, A+ T" a, c4 L
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
4 u) d y9 G3 R. @the emergence of clonal T cell populations, were observed both in one patient
/ @( i. h8 Q$ j3 }: W/ a0 t: Twho relapsed and in one patient in remission. Our results suggest that the
, m4 J- b; t0 u5 j7 z6 H; b+ Vcharacteristics of complete molecular response on dasatinib treatment may be
' A7 \8 c F- L" `: Vsimilar to that achieved with imatinib, at least in patients with adverse+ d3 Z5 `6 ?( @* f, `
disease features.
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