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。
' o) M& a" g& x2 r6 w4 X 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。" e! S! @+ S( V- @. a2 D W! p
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作者:来自澳大利亚 U" Q; w5 ^7 ]
来源:Haematologica. 2011.8.9.7 x% r1 I2 i/ O3 I
Dear Group,( N: m( `% _) Y6 K
( @ ]) o# Y1 G, R0 _Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML. e2 p4 H! \! S) |6 P8 V) @, g4 {
therapies. Here is a report from Australia on 3 patients who went off Sprycel
; u, K+ Q, l* Y' H7 N- R+ [* Bafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients4 |- W! o/ \" h5 V5 C& z! B- I
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
) O9 q& p1 [2 A1 }, R! |does spike up the immune system so I hope more reports come out on this issue.3 j% o' h" K, C( U7 i
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The remarkable news about Sprycel cessation is that all 3 patients had failed- O" g& P/ C" x" I2 f0 C
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
1 j- P' Q! B( A0 Z8 mdifferent from the stopping Gleevec trial in France which only targets patients
4 a5 F7 u8 `$ U- W1 s, R7 Owho have done well on Gleevec." l9 `$ x' p6 |4 S
2 |0 _. W2 ~0 a% r! }0 yHopefully, the doctors will report on a larger study and long-term to see if the
; q( t2 D" L( y- {4 Wresponse off Sprycel is sustained.( Q Y) P; s- C: I# v+ h- ~4 o' S
* w+ Y7 J' z! n9 L* i: R# wBest Wishes,
% M9 B0 y% T- w4 S" n1 y; hAnjana
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: H0 {3 U+ h- c' \Haematologica. 2011 Aug 9. [Epub ahead of print]
$ A$ U Z6 g9 N+ u" }Durable complete molecular remission of chronic myeloid leukemia following- @) V% }5 z: m- e8 b) ]( F
dasatinib cessation, despite adverse disease features.7 ?; `7 Y) B( z
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.0 F+ V+ n" i A* T9 B- {; b
Source; E5 d' U, u/ e1 a- ^
Adelaide, Australia;
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0 j$ u1 A! P4 c# X8 l: MAbstract- j, t9 s# Q1 f
Patients with chronic myeloid leukemia, treated with imatinib, who have a
8 S3 ^# H) y2 J* d' a! Rdurable complete molecular response might remain in CMR after stopping
1 t( ]2 k- C% Y0 n+ E% _0 W! \treatment. Previous reports of patients stopping treatment in complete molecular1 P3 M( p3 y- o6 O" R, b/ ]
response have included only patients with a good response to imatinib. We
, z3 m4 B8 p! v8 N& l0 j) g3 vdescribe three patients with stable complete molecular response on dasatinib0 | ~7 E n, p& n
treatment following imatinib failure. Two of the three patients remain in8 H& i) \1 m# U. x; s! H6 [
complete molecular response more than 12 months after stopping dasatinib. In* f: D0 e4 A7 [" A
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& H- W d5 r; H2 k& |7 e
show that the leukemic clone remains detectable, as we have previously shown in( U1 W$ G( k1 t, O& s- ~& n
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 {" G6 K! l% g+ f# ]8 F5 z4 N
the emergence of clonal T cell populations, were observed both in one patient" G2 m! r$ C9 u J! d4 {# L5 i
who relapsed and in one patient in remission. Our results suggest that the
( c2 l) s" f3 U1 f2 Mcharacteristics of complete molecular response on dasatinib treatment may be
4 l+ g5 P: @; h4 T' qsimilar to that achieved with imatinib, at least in patients with adverse: O/ J ?$ e4 q' i* w @
disease features.
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