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。+ J# w) H# g: X5 i0 y
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。
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作者:来自澳大利亚
! l' O7 b; P6 c1 Q, x1 H来源:Haematologica. 2011.8.9.5 i: l; _2 _, @* A6 O
Dear Group,& m' {* j: K5 m; D! W/ N5 ^1 g
7 J# T, d, X7 t% X. v$ BSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML! D" ~5 X Q- ?9 [8 i
therapies. Here is a report from Australia on 3 patients who went off Sprycel
* |' N! g! [. |7 u, ^3 l8 n1 ~" lafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients" q8 x$ y% x9 d l; @0 J4 A
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
+ a4 S( R, e: _does 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 failed6 j0 t/ P. g6 k
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
7 h. j, O+ {( G; a1 Kdifferent from the stopping Gleevec trial in France which only targets patients
! z1 [* V, Q1 [, ` xwho have done well on Gleevec.2 ]3 h/ L" i j
. e( E7 z) z' s2 X3 h8 E; lHopefully, the doctors will report on a larger study and long-term to see if the
3 ]% W c6 ~/ b) _) l, jresponse off Sprycel is sustained.
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Best Wishes,9 b h4 R. ~& p" N7 Z* {: N( c
Anjana$ r7 D, s2 F" o8 n! S, t- k, J7 m
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Haematologica. 2011 Aug 9. [Epub ahead of print]
4 P( n3 `% q. U4 J, O4 P' A$ m; xDurable complete molecular remission of chronic myeloid leukemia following0 Z0 c7 d. `, Z" z; N- q* ^7 o
dasatinib cessation, despite adverse disease features.- Q5 d, P6 H" ~. x
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;+ H, G C! U# H7 o; J
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Abstract8 j5 Z9 I I! B' T, Y# o, R
Patients with chronic myeloid leukemia, treated with imatinib, who have a$ A5 U: C9 H& E- h
durable complete molecular response might remain in CMR after stopping
, a$ {! l$ X- `; }treatment. Previous reports of patients stopping treatment in complete molecular, f2 Q2 M( v# B' X! S* u
response have included only patients with a good response to imatinib. We
' A/ j/ i4 {+ `, \7 \' a4 K2 |/ ?, idescribe three patients with stable complete molecular response on dasatinib) X+ Z: y3 a! G9 w9 L% `7 u+ R" D
treatment following imatinib failure. Two of the three patients remain in+ n4 Y* V8 z8 F, h4 U; Y
complete molecular response more than 12 months after stopping dasatinib. In
# u2 K: P! I5 g! _; Dthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to" K; ]) h. \) ~' A7 K
show that the leukemic clone remains detectable, as we have previously shown in1 p C8 X$ _- B( t2 {1 q2 {
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
! ^3 w# t8 G' I) |) Dthe emergence of clonal T cell populations, were observed both in one patient
# z; ~1 R, k- E$ fwho relapsed and in one patient in remission. Our results suggest that the3 q$ C9 B1 Q9 g" U
characteristics of complete molecular response on dasatinib treatment may be3 M9 k' e# @% ]" Y! L, @
similar to that achieved with imatinib, at least in patients with adverse: G8 d+ z% V" V8 J
disease features.
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