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 a$ R1 t- O4 @/ @2 B; H
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。4 S' j8 E* f6 l8 p
; q2 K+ l7 Q# ]% W4 m8 s1 [9 ?作者:来自澳大利亚
8 _% E' ?* q$ x) \. ?; j5 }8 Q+ G5 G来源:Haematologica. 2011.8.9.( E: Z8 l3 v* H G
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML P. A9 W/ z. [7 p0 ]# _
therapies. Here is a report from Australia on 3 patients who went off Sprycel% Z7 s6 X3 R: x
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
* ^7 F! u( ^! r1 ]- Z$ ?( W: i$ premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' V" _% M3 \8 |. x" b; F0 l/ d- I
does spike up the immune system so I hope more reports come out on this issue.
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. [! t7 ]/ L. z5 K" \4 @# A! R9 \The remarkable news about Sprycel cessation is that all 3 patients had failed% ^0 Q: {( E/ n1 }! t& Y
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
8 B: p T/ {4 a/ S/ c4 J6 g# idifferent from the stopping Gleevec trial in France which only targets patients
& ~0 f8 t, a& e" k8 [4 iwho have done well on Gleevec.: B# B0 e8 A: o% N
; A* x4 k' c6 F6 u9 J' q0 EHopefully, the doctors will report on a larger study and long-term to see if the# {% |! [! N4 f
response off Sprycel is sustained.
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Best Wishes,
6 z' r# P& [0 H* {' _Anjana9 [) ?1 E0 N6 W! Y
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. m8 _2 U( J' @( H8 L& e
7 d9 Y' i: ?* Q9 A, M) fHaematologica. 2011 Aug 9. [Epub ahead of print]
% {- q4 h9 H' _" \Durable complete molecular remission of chronic myeloid leukemia following
& A2 s3 }- i, `) j* N- Zdasatinib cessation, despite adverse disease features.
* a. a0 }- k. ?3 ~* Z2 j8 E, mRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;
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Abstract: c; n; A+ \+ \0 a5 l4 ]
Patients with chronic myeloid leukemia, treated with imatinib, who have a
' Z! i1 h" \4 y' \' fdurable complete molecular response might remain in CMR after stopping6 J+ |" i/ K) N& H) {9 c @8 O
treatment. Previous reports of patients stopping treatment in complete molecular& f2 Z. w/ p6 t: o+ U2 G
response have included only patients with a good response to imatinib. We
- G+ ^, z' e2 E% q& d$ _& t4 \describe three patients with stable complete molecular response on dasatinib
' ~/ c+ t D3 D! z" c% ?$ X, Btreatment following imatinib failure. Two of the three patients remain in1 ~. z3 u b% F2 X. y1 I. ?. @/ O
complete molecular response more than 12 months after stopping dasatinib. In3 E7 E( i9 O9 a3 B% W0 I+ b
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, `+ Y9 l& \1 |1 G% ?9 a: S! g
show that the leukemic clone remains detectable, as we have previously shown in
' `& P- F4 k* |& eimatinib-treated patients. Dasatinib-associated immunological phenomena, such as& e8 f: U# q! v& s+ a
the emergence of clonal T cell populations, were observed both in one patient( T4 }2 R2 F7 ]) p T0 t% Q* J X
who relapsed and in one patient in remission. Our results suggest that the
$ ~6 q2 p1 o+ U: Kcharacteristics of complete molecular response on dasatinib treatment may be; E" e; p3 M# y/ r: x3 \
similar to that achieved with imatinib, at least in patients with adverse
. p1 G3 Q; j: J( ]5 u/ ~- ydisease features.
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