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。, e& ^) m. f: n* ~! q5 o) v& E( m; 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。, L' }8 Y8 r5 t. i7 F1 F! L
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作者:来自澳大利亚0 G$ Q- N3 w' }) _0 s# U8 n0 c9 O
来源:Haematologica. 2011.8.9.! E# O* q7 D1 X6 B" H2 [
Dear Group,9 ]( y- t3 J9 a; s( H
# J$ K/ w$ @, ]+ ASome of you are on Dasatinib (Sprycel) and we wish to give news on all CML% f$ p# O D9 y2 V# U! o3 O" x7 s
therapies. Here is a report from Australia on 3 patients who went off Sprycel
7 ], n/ U# b6 u4 Z, \( s; A! w2 G/ eafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 O$ x5 }' T3 b dremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
0 F. Q' L) Z/ B f" g7 @* f. ydoes spike up the immune system so I hope more reports come out on this issue.7 ~" s& N# U5 x7 v9 q: l' z
b2 N9 @& B7 f# u+ X2 ~3 F( {3 Q4 o. [The remarkable news about Sprycel cessation is that all 3 patients had failed( T8 K' U- [2 @( A" e0 @8 f( S
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
+ S# t+ d T# Y( s _# U2 ]different from the stopping Gleevec trial in France which only targets patients& e) g, P* ?; @2 f. n, ?4 \. e
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the8 G1 H8 U1 O. ] o
response off Sprycel is sustained.9 {# J* v! P& v% A4 n- V1 g& N
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Best Wishes,4 g' [# r) L0 y1 Y h0 X- z3 ^
Anjana7 \7 m) E+ d: m0 i+ {4 t+ a+ d
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Haematologica. 2011 Aug 9. [Epub ahead of print]5 H: G9 I4 X: [* @" k
Durable complete molecular remission of chronic myeloid leukemia following
' P! C, ?1 s+ e* S4 U. I- _3 fdasatinib cessation, despite adverse disease features.! R0 w3 s* _' X/ e( S6 s
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 c7 G* j: H4 {6 p) p/ ~+ V5 j
Source$ s& H! ?" q$ f4 D: b' D
Adelaide, Australia;
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Abstract
4 P; |# M4 n! z6 xPatients with chronic myeloid leukemia, treated with imatinib, who have a8 ~! a7 \. ~* V! x+ O! z O9 P
durable complete molecular response might remain in CMR after stopping
$ h: U- C+ u! _) Vtreatment. Previous reports of patients stopping treatment in complete molecular
# B# s8 I# ?; K& }! {response have included only patients with a good response to imatinib. We
/ l( l2 \4 }1 gdescribe three patients with stable complete molecular response on dasatinib
: }& d3 E* S; t, \9 c5 dtreatment following imatinib failure. Two of the three patients remain in* o1 T3 M7 ? \' Q
complete molecular response more than 12 months after stopping dasatinib. In
% D0 l/ z( v m# Fthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to# t' g8 N% F; X! s4 l; q
show that the leukemic clone remains detectable, as we have previously shown in2 t, }, i; g! D, }
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
. }( q' W2 @' d- p$ x1 C# u, Fthe emergence of clonal T cell populations, were observed both in one patient
6 ~4 U6 V3 B- @9 e& [" Y: P, pwho relapsed and in one patient in remission. Our results suggest that the* C. T1 ]8 k4 a$ O: ]
characteristics of complete molecular response on dasatinib treatment may be) W+ U4 T% c. ~* }- _: s
similar to that achieved with imatinib, at least in patients with adverse- d% ~6 k' A! N8 w& Q |$ a
disease features.3 Y7 d- B" g7 ^* {4 e: {
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