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。* H: X) ?' _7 Y. F+ W
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9 H3 z7 q( K8 D: I
来源：Haematologica. 2011.8.9.
. C+ f \) @3 P1 iDear Group,
! f0 e) J! r' i1 d* \6 N
7 E: x& h( h* ?. e4 |Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 g8 u( D* v0 K a% n3 E3 @7 o6 q
therapies. Here is a report from Australia on 3 patients who went off Sprycel
. Y1 J! h" i5 k: zafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients2 W$ w( K$ m- o! [# i
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
0 z' D9 I5 S sdoes spike up the immune system so I hope more reports come out on this issue.; }& G N% E1 d* F& H5 f, ]
% q* W$ ?& j! L, `+ D# h* @. ] H
The remarkable news about Sprycel cessation is that all 3 patients had failed
' ]- e6 q9 A, j ~+ N4 t4 UGleevec and Sprycel was their second TKI so they had resistant disease. This is& F0 ]5 ~, j# Q
different from the stopping Gleevec trial in France which only targets patients1 i7 h+ `- c1 R
who have done well on Gleevec.
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' m" W( n" J& v3 N: Q1 V# NHopefully, the doctors will report on a larger study and long-term to see if the0 Z) e4 N6 z$ f- {; S( u2 ]* k
response off Sprycel is sustained.0 h! a5 M% D$ f8 i' v
4 q, q: j" F. }! H6 S& S
Best Wishes,
( ?) ]( Y0 l/ {+ M( E% \6 OAnjana
! Q2 T8 ]' t2 g9 R/ i/ v0 A0 Z
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& q6 M. U, Y% [1 Y/ x+ {$ `3 d
Haematologica. 2011 Aug 9. [Epub ahead of print]! o) F3 [ a9 `4 [ i
Durable complete molecular remission of chronic myeloid leukemia following
) ?1 C. i0 l8 H. f& Y, p( sdasatinib cessation, despite adverse disease features.
: t- e: E# ^( Q# Q0 s5 U1 d, TRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
3 d+ ]' R5 w: s2 u( gSource) r& t) y# [/ \; s. q6 \
Adelaide, Australia;4 [ x: R6 G$ k
& N, v+ B `# Y7 }% h& ]Abstract
" y) }/ C9 B1 x) qPatients with chronic myeloid leukemia, treated with imatinib, who have a
; w7 [3 J- F/ d6 `durable complete molecular response might remain in CMR after stopping9 b3 x$ Y2 [9 g; g8 P
treatment. Previous reports of patients stopping treatment in complete molecular
0 Q0 X- k/ M* Z g0 d/ J' E) u2 I, v3 Oresponse have included only patients with a good response to imatinib. We6 [9 T& R* U6 p$ z
describe three patients with stable complete molecular response on dasatinib+ o/ l, W, R. s
treatment following imatinib failure. Two of the three patients remain in' F+ \- Y5 C8 A4 `& N4 i& G: q, [
complete molecular response more than 12 months after stopping dasatinib. In$ O! T! I( V3 E2 i
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
% e: g, E" b: C" Wshow that the leukemic clone remains detectable, as we have previously shown in
/ K6 f+ c4 Y/ o% Dimatinib-treated patients. Dasatinib-associated immunological phenomena, such as2 A+ D9 E6 n0 E l" C) S! c# z9 H
the emergence of clonal T cell populations, were observed both in one patient. S8 j9 `9 I" b- g3 r/ ]
who relapsed and in one patient in remission. Our results suggest that the
& C* ?. {8 U* {9 K: ocharacteristics of complete molecular response on dasatinib treatment may be
& o4 N o- }/ |: n' x' csimilar to that achieved with imatinib, at least in patients with adverse. U- Y6 A. R+ ~, A
disease features. w) S/ q' w/ ~5 ~
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