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。
1 [% `8 T8 f) ~" u3 j, o6 \ 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。8 L! e" H+ c6 K( R- z# c) ]3 R* _
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作者:来自澳大利亚
4 Y, o! t" x; q' `来源:Haematologica. 2011.8.9.
8 O' E/ s2 \' SDear Group,' W. ]) E4 o4 B# Q; s+ U: P
" T8 Q5 d4 T+ [# d! {1 S0 Z: X2 r1 ySome of you are on Dasatinib (Sprycel) and we wish to give news on all CML6 p* K* A$ i3 K3 L# l
therapies. Here is a report from Australia on 3 patients who went off Sprycel
' {; A% F6 T2 l1 w f2 safter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 m" }# a$ C) j+ Tremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel) u7 w( X1 ^% d: X0 S) @
does spike up the immune system so I hope more reports come out on this issue.
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! r6 O. _7 O& _2 P4 Z% Q* ?6 |: zThe remarkable news about Sprycel cessation is that all 3 patients had failed, c0 _/ c, d @/ F4 l' \+ W7 k/ g8 `
Gleevec and Sprycel was their second TKI so they had resistant disease. This is2 A- X% z+ n4 b9 W+ B
different from the stopping Gleevec trial in France which only targets patients) |6 q( O! B; n/ m! {) q' 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
' {- r8 B0 y5 {+ A% w9 g) `. U* iresponse off Sprycel is sustained.4 x) g* f& O" C) g J1 e
, x: S. C- y6 r0 dBest Wishes,
3 k4 G" J6 M% j2 E/ L; n. yAnjana
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1 ]7 q5 a( [1 q$ A$ G5 b9 d+ uHaematologica. 2011 Aug 9. [Epub ahead of print]
) f$ Q. ?$ o8 u+ b3 j& cDurable complete molecular remission of chronic myeloid leukemia following" R; c( f- t- j- I i
dasatinib cessation, despite adverse disease features.
, b" n7 c( y. ?7 jRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ e4 h' g, Z0 }& {# r
Source0 e0 k4 g1 u0 H% Y; j w
Adelaide, Australia;# V; w2 Q. B/ `* R! b" J
. B, q( _: D2 {- u; }9 C! q( uAbstract
( m6 V& R7 h% D" _, e1 mPatients with chronic myeloid leukemia, treated with imatinib, who have a
8 m( G4 `- j: h2 c [* ~& a* `- Vdurable complete molecular response might remain in CMR after stopping- x" i2 n: i# ~1 p
treatment. Previous reports of patients stopping treatment in complete molecular8 s O1 o( M6 u7 d# ~8 a+ Y
response have included only patients with a good response to imatinib. We/ [9 |/ A3 o0 U( X: |1 w' K5 y- b
describe three patients with stable complete molecular response on dasatinib
8 X5 G7 Q+ F" k* Ctreatment following imatinib failure. Two of the three patients remain in- d% h1 T1 P; P3 ]
complete molecular response more than 12 months after stopping dasatinib. In
, N$ \) w6 K' b/ x( `) @- Othese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, c1 j+ ?. i/ e( b4 R' O
show that the leukemic clone remains detectable, as we have previously shown in4 L) h( j% g4 G! h6 m, K
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as2 c3 n. Z- A: I$ g' H8 X
the emergence of clonal T cell populations, were observed both in one patient7 k6 B- m8 h' G1 }
who relapsed and in one patient in remission. Our results suggest that the h7 ^3 g. e$ [ c
characteristics of complete molecular response on dasatinib treatment may be+ s( G q r1 u
similar to that achieved with imatinib, at least in patients with adverse
; j3 }7 w8 Y/ r' v3 s: j$ xdisease features.4 R/ r) h/ K- ]
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