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 Y# ?. L/ e: k( X& c
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。/ m" F. U& t! x* J) G4 A" Q, I
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作者:来自澳大利亚* u, a9 t4 |' F* s& v* G. a% C
来源:Haematologica. 2011.8.9.
9 W$ C/ U% |: t) Z3 e& PDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
3 v2 i6 y- \1 r0 wtherapies. Here is a report from Australia on 3 patients who went off Sprycel
( B7 H, H$ {, ~1 F( ]+ ~after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients; L; u0 n6 D" d; ?3 c4 g! T# @) Q
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
( O$ C' c4 B' ~/ k! Udoes 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
. W+ N0 _& E& `. C! Z8 A, B9 `Gleevec and Sprycel was their second TKI so they had resistant disease. This is
. B# l( u& T$ ` M( x) A k5 s$ g' wdifferent from the stopping Gleevec trial in France which only targets patients2 M1 j7 C! o% t9 ]+ I9 S0 E* F
who have done well on Gleevec.
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9 ]1 x# t. e( S# @$ |6 FHopefully, the doctors will report on a larger study and long-term to see if the
- u1 e6 I$ A5 ~, j) ~3 G' I: qresponse off Sprycel is sustained.
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! u" q3 l* {6 e0 e; eBest Wishes,
& t) ^8 ]+ e4 j4 x2 H: WAnjana; E; o/ v: ^! F/ \
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Haematologica. 2011 Aug 9. [Epub ahead of print]
+ o2 `% k7 F6 n- j2 |6 ?Durable complete molecular remission of chronic myeloid leukemia following7 k) }" B1 c1 G) ?
dasatinib cessation, despite adverse disease features.; B& i Y2 @7 p2 [& J3 P: B
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 v6 F H' X- M
Source
U+ R }) N; @% f6 w9 XAdelaide, Australia;& ^* ?% h6 D+ C' W
- P. c- M# p8 s$ l! x1 W- B% J; rAbstract
( Y) [; c& k0 K$ n# \* G R! fPatients with chronic myeloid leukemia, treated with imatinib, who have a
9 C1 x/ h0 A$ Z' N6 \durable complete molecular response might remain in CMR after stopping3 c8 Z3 i$ {+ [1 W* E o
treatment. Previous reports of patients stopping treatment in complete molecular
( }" h. s: k3 @0 cresponse have included only patients with a good response to imatinib. We
K4 _' z8 F$ e1 K5 {describe three patients with stable complete molecular response on dasatinib
" q( e* K9 G4 R2 y* b, Ftreatment following imatinib failure. Two of the three patients remain in
; n- Z3 Q! T$ m' K0 rcomplete molecular response more than 12 months after stopping dasatinib. In
7 d4 F4 Q$ G0 kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& H1 A0 V% x& E* i7 E
show that the leukemic clone remains detectable, as we have previously shown in: B$ N3 j& t1 L0 \' `! v3 _
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
' @/ o/ B' h! }8 r( h8 {" q" V' H$ m' Rthe emergence of clonal T cell populations, were observed both in one patient
* {' W8 ^9 r8 i0 Q* m* Qwho relapsed and in one patient in remission. Our results suggest that the
6 @) r1 J! F2 a; Pcharacteristics of complete molecular response on dasatinib treatment may be
) C. g) S2 w' L$ t) Q5 z* r" Zsimilar to that achieved with imatinib, at least in patients with adverse- Q$ _1 e$ I& C. S- C+ u
disease features.
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