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。6 C0 `$ v7 a6 T+ ^* t B' n) 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。% q+ J/ j8 S1 j# `& e% R. p) d$ J
. W+ j( J2 P: G( s作者:来自澳大利亚
% W1 ?- o8 V2 i: [" K" a" s* v S来源:Haematologica. 2011.8.9.
: I/ b3 h. u+ c b' x5 iDear Group,
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5 n% ~% r) i, [# k) u, C2 a' } \) PSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
0 I. |' c' K0 Etherapies. Here is a report from Australia on 3 patients who went off Sprycel; D' q4 p7 G e. V* {* O- T
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 u+ v5 G# R6 \6 y* c: rremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
/ @( k, W* V3 n) P+ N) B/ a- adoes spike up the immune system so I hope more reports come out on this issue.
: b4 W6 c$ \" ?1 _, ^" s9 Q
7 a' l0 W5 ~% O/ pThe remarkable news about Sprycel cessation is that all 3 patients had failed
/ C4 @: K* i# p# M0 C! v4 D0 IGleevec and Sprycel was their second TKI so they had resistant disease. This is
4 j3 \* i1 {3 Mdifferent from the stopping Gleevec trial in France which only targets patients/ I6 {9 R2 K! C
who have done well on Gleevec.
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; A) ^' Q J, R2 T, Y+ B: D' _) UHopefully, the doctors will report on a larger study and long-term to see if the
, s5 p2 i$ L+ k, C- i3 Gresponse off Sprycel is sustained.
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Best Wishes,
# Q6 A6 `: Q, V# d1 Q% wAnjana
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( D! i% b, \8 o4 Z8 bHaematologica. 2011 Aug 9. [Epub ahead of print]
V, F" f P8 v7 nDurable complete molecular remission of chronic myeloid leukemia following
$ T7 A* V8 }6 Z4 `0 Sdasatinib cessation, despite adverse disease features.) h7 K. G! H/ W& T& h' x& {
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' m |- y. A5 b- c# Y5 L7 A k! k
Source1 A; a) J8 L& T5 I: K: ]% \
Adelaide, Australia;
3 i; K o- U$ X) e* o" a6 {. k/ o6 H ]; \+ D
Abstract6 M) @2 y3 x$ i. D
Patients with chronic myeloid leukemia, treated with imatinib, who have a
/ K$ I! J$ e' M" Kdurable complete molecular response might remain in CMR after stopping& Q! L2 A* P9 o+ ~) I* b
treatment. Previous reports of patients stopping treatment in complete molecular
) ]. [6 r- ^- A- }# Qresponse have included only patients with a good response to imatinib. We2 B: u, U+ Z. y9 x5 `5 m
describe three patients with stable complete molecular response on dasatinib: c& p& }; ~" G. P
treatment following imatinib failure. Two of the three patients remain in
7 S6 x5 x' F/ k! fcomplete molecular response more than 12 months after stopping dasatinib. In# g- o- ], d' ?9 p
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& E* l1 n- `* p, y! I% ]$ I
show that the leukemic clone remains detectable, as we have previously shown in# T& g! p# i( p' n; C/ K! _
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 g. n/ g( z3 T: _( x& z
the emergence of clonal T cell populations, were observed both in one patient+ R7 P5 f& E/ r7 p# C/ M8 @' ]
who relapsed and in one patient in remission. Our results suggest that the3 f. E" ~1 L& o& ?& ]) s
characteristics of complete molecular response on dasatinib treatment may be
% J# a% [* S" O' D w0 {: xsimilar to that achieved with imatinib, at least in patients with adverse, L7 [- t8 R' P& U% v
disease features.- |( K* ?$ v I3 ?+ S$ j2 ^
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