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。
9 w5 F+ Q% L0 ] c+ x- ^7 {, V M 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。( G+ N5 J' B' b s! Y
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作者:来自澳大利亚
$ I4 z7 O+ _8 l& |7 l4 s来源:Haematologica. 2011.8.9.
) a+ |' a2 O" m0 A9 GDear Group,6 f9 h% h7 y. y7 S, R7 G P: ]2 S
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML- O; q6 Q, h6 r& u6 V: M# c
therapies. Here is a report from Australia on 3 patients who went off Sprycel) b7 q8 |' l6 B0 p( I
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients/ l2 L$ Q/ Z. \1 K3 w1 n: p
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
7 a* m& `9 t( }: e1 [5 Sdoes 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
: Y) b$ E0 p5 ?! \. L7 |Gleevec and Sprycel was their second TKI so they had resistant disease. This is A! f; q7 G1 i
different from the stopping Gleevec trial in France which only targets patients
- V+ G V% d0 T0 g2 iwho have done well on Gleevec.9 X1 E* |& W7 u" Y7 N) [* q. j3 c1 a
% s4 @9 `6 ^2 J1 p8 J. EHopefully, the doctors will report on a larger study and long-term to see if the8 x. F/ I" J/ _1 X" q! q
response off Sprycel is sustained.
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Best Wishes,( b. c! g) W( j0 J
Anjana% _& \* j$ A |" V2 i8 `7 L
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Haematologica. 2011 Aug 9. [Epub ahead of print]) l5 [* G. @- D4 H, P
Durable complete molecular remission of chronic myeloid leukemia following
z/ A$ q! r/ M3 b5 Adasatinib cessation, despite adverse disease features.
/ z+ F7 p( D( c, C$ O; }" [Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
3 c# D, x9 \4 ~6 gSource
' ]) o$ l- s+ U- R5 HAdelaide, Australia;
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" D' V: D4 v/ EAbstract G3 g6 m3 `4 ^$ g
Patients with chronic myeloid leukemia, treated with imatinib, who have a9 W/ S0 {) {3 r' g
durable complete molecular response might remain in CMR after stopping# A5 V% m$ ^- j9 _" c
treatment. Previous reports of patients stopping treatment in complete molecular# p/ w% W5 T( @) `. h C
response have included only patients with a good response to imatinib. We1 a! M6 [1 z4 _# l
describe three patients with stable complete molecular response on dasatinib. W j5 v5 t, \4 q5 I$ N+ P
treatment following imatinib failure. Two of the three patients remain in
1 I7 g, p- M7 D+ b" K6 ?complete molecular response more than 12 months after stopping dasatinib. In
! x' V( \# Y# @" kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
$ c) c, M" M. ]- s' T/ L2 b5 bshow that the leukemic clone remains detectable, as we have previously shown in
$ \. \2 E. C6 H2 @$ d& Rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as+ q" f2 O6 Y3 C( @: o
the emergence of clonal T cell populations, were observed both in one patient
* m; w3 v& p9 j$ Dwho relapsed and in one patient in remission. Our results suggest that the
4 O& G) c! }& W1 B* v2 r: u; Hcharacteristics of complete molecular response on dasatinib treatment may be
( W0 Y# }9 S1 L) V2 csimilar to that achieved with imatinib, at least in patients with adverse
* Y0 }9 ]% K2 x7 b5 Y: q2 R: Idisease features.
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