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。7 X; ]8 Q3 F( g' E1 x3 I1 j
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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, @! X1 k; l5 r* \4 u作者:来自澳大利亚
2 c- ?3 q8 |2 R. Y2 Z0 s2 S来源:Haematologica. 2011.8.9.
1 T. B( S$ {; k7 T& iDear Group,9 i/ P O/ [/ j7 ^ r# i
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ ? ?4 M; W! _6 z# a" z, F" Z
therapies. Here is a report from Australia on 3 patients who went off Sprycel8 a5 L7 A# b: l4 @% \; x
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 i& s* w6 L: q# b. Aremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
% U0 c2 x7 V" }does spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed: @0 b4 p( E1 b$ g, u$ N6 m* O* a
Gleevec and Sprycel was their second TKI so they had resistant disease. This is4 I: ]/ D; h& ?6 R( l0 \& J
different from the stopping Gleevec trial in France which only targets patients
' g# b2 g9 Q# s; E3 K' ~% U: wwho have done well on Gleevec.
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6 R3 Z7 K$ d/ u* a" @, hHopefully, the doctors will report on a larger study and long-term to see if the7 T( m2 U' R; H6 |: T
response off Sprycel is sustained.
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Best Wishes,9 K* ^4 C/ d7 M
Anjana( E9 m: a. H" U" W( o+ m3 A
q$ o) w, E" l! K
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# D! k% \: b1 r- W5 U0 e8 }$ UHaematologica. 2011 Aug 9. [Epub ahead of print]
: U; G9 @: [+ pDurable complete molecular remission of chronic myeloid leukemia following
/ h/ C0 |9 \! v3 [4 Jdasatinib cessation, despite adverse disease features.3 i1 y: X, }& C0 x& Z- N7 @
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.! n1 q# n4 `2 r2 m, J: A
Source4 m; _5 ~: C) \1 u1 @& i
Adelaide, Australia;
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Abstract
4 r4 Q2 N% i4 M3 g3 J% E2 v( L/ tPatients with chronic myeloid leukemia, treated with imatinib, who have a
7 d, P9 ^) Q7 x. Kdurable complete molecular response might remain in CMR after stopping& u; z8 g9 G7 H, I1 J6 U
treatment. Previous reports of patients stopping treatment in complete molecular( i& z6 Q i: N) S7 x$ D
response have included only patients with a good response to imatinib. We
+ o# e0 J: ?6 }( ~. T% Sdescribe three patients with stable complete molecular response on dasatinib! C2 M5 d E. n" u& W( B
treatment following imatinib failure. Two of the three patients remain in
. t* f! W) p$ qcomplete molecular response more than 12 months after stopping dasatinib. In
! `% h8 q+ K! z. O F% Ethese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
- n, ~" n2 `$ R( _show that the leukemic clone remains detectable, as we have previously shown in
5 e' c5 L! d: k+ nimatinib-treated patients. Dasatinib-associated immunological phenomena, such as* c; t- K& `9 p
the emergence of clonal T cell populations, were observed both in one patient6 p" |9 L: }# M& V8 p: L1 o
who relapsed and in one patient in remission. Our results suggest that the' C4 B4 l" x) d3 `) a1 L u1 X
characteristics of complete molecular response on dasatinib treatment may be
0 o% m+ z/ N" \% lsimilar to that achieved with imatinib, at least in patients with adverse
: S9 F$ T! g2 f1 x9 N7 C$ Wdisease features.
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