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。: b* H; h: {& `0 J, f9 g% f
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。5 V" d/ V) |; Q' I7 V1 h0 @# n
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作者:来自澳大利亚9 \+ t. I7 ?4 X
来源:Haematologica. 2011.8.9.& C+ Z# O5 b' i2 W8 w" h
Dear Group,
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1 v9 i! L0 n# Y$ H$ {Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: o i$ |- s1 J# P7 @/ Etherapies. Here is a report from Australia on 3 patients who went off Sprycel: ~6 b, H9 `" s. N& Y# ?
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients/ J/ E! C |( U. L( @' @7 n- z V% _0 o
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel7 @+ s. H9 z6 \* o5 C7 |. R0 x
does spike up the immune system so I hope more reports come out on this issue.7 O; H; p& S. X2 L$ N+ `+ P
9 t5 D3 x, a- z4 H+ q8 i. o5 ]$ ZThe remarkable news about Sprycel cessation is that all 3 patients had failed
+ `# }: M& f& iGleevec and Sprycel was their second TKI so they had resistant disease. This is9 t" F1 [9 R+ f% L$ G9 E5 s( ^. \8 y
different from the stopping Gleevec trial in France which only targets patients
2 j9 { d7 \6 D) ~' O: o% nwho have done well on Gleevec.
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& C, _; D* E7 l! {2 o' T, l7 q7 ~Hopefully, the doctors will report on a larger study and long-term to see if the
; b5 X A& [* Z! G, U# P- aresponse off Sprycel is sustained.6 O) i- F3 U" m4 | ?
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Best Wishes,! f0 f3 |$ X/ u& W% V4 D8 Z; c- g
Anjana9 S5 c( V7 v* K, |9 {) _( n
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: F; E( t4 k1 Q4 f& l0 \* W8 IHaematologica. 2011 Aug 9. [Epub ahead of print]6 u, z7 d2 r/ c4 y* I+ Z T
Durable complete molecular remission of chronic myeloid leukemia following
3 w& O6 t2 w4 n# `( t: Rdasatinib cessation, despite adverse disease features.4 c Q5 [5 M, Y d6 N0 X& y
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
! y) r1 j, v e: {" LSource
* d- O7 R! j+ `7 S4 VAdelaide, Australia;/ U$ h* s2 I+ `/ |9 P! i
8 Y/ g6 X( d$ v, T, a4 @, o5 QAbstract$ ~# {6 u& h6 T
Patients with chronic myeloid leukemia, treated with imatinib, who have a
, p( d* f# _4 J' R) vdurable complete molecular response might remain in CMR after stopping
/ u* N$ e+ H8 F. Itreatment. Previous reports of patients stopping treatment in complete molecular: j0 ^/ u& ?8 J) _- D; c) B. \
response have included only patients with a good response to imatinib. We
; m/ u+ O; p6 A, ndescribe three patients with stable complete molecular response on dasatinib
0 X1 R; V; o6 l- f: b+ n1 z' N! Ctreatment following imatinib failure. Two of the three patients remain in
4 b4 e! `! I0 n4 E# \complete molecular response more than 12 months after stopping dasatinib. In0 B: G+ p2 z% E. b& M; Y( [ f9 R
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to9 K$ F' g# \3 Z8 m& Q" a; b: ~
show that the leukemic clone remains detectable, as we have previously shown in2 ~+ v% }, L( y6 c% W( I$ {
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
# K$ X; x8 V: \: D" H3 k( o& Bthe emergence of clonal T cell populations, were observed both in one patient
6 y, h5 d: F1 z' Cwho relapsed and in one patient in remission. Our results suggest that the$ s$ x" t: T, M, X; q! i
characteristics of complete molecular response on dasatinib treatment may be
2 ?$ q, Q6 }* ]5 J; R; T; asimilar to that achieved with imatinib, at least in patients with adverse
' M* r+ N8 r2 {8 qdisease features.
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