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。
5 R" G- R; `' z! }. [ 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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2 G& ?( h# R) R- g- h' a& ?作者:来自澳大利亚+ l/ B$ v* ], {, c- \- @4 ?$ U
来源:Haematologica. 2011.8.9.. ~- ]% q& ~# h: f7 ]! h
Dear Group,0 U( [+ h1 q! {5 [, _; ^
1 X$ ?5 R5 X. g4 r: SSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
) y! v. V. U4 M" @3 Utherapies. Here is a report from Australia on 3 patients who went off Sprycel
1 C% W9 O* Z' Z C3 j; oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients. _# V5 Y2 v0 q: {) ?" }
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( m/ {& A. l, S; s3 |$ ?$ M
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 failed2 {' w3 y- X" g
Gleevec and Sprycel was their second TKI so they had resistant disease. This is' @) Z9 N% w4 i- d; P; Q
different from the stopping Gleevec trial in France which only targets patients
4 @) m2 z+ ?9 `8 E2 _* ^who have done well on Gleevec.
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& C' ~6 M0 \# R! D& C# NHopefully, the doctors will report on a larger study and long-term to see if the, r3 J5 f- a2 S1 R
response off Sprycel is sustained.
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Best Wishes,
$ D, ], q. K" ?/ \5 BAnjana
4 `# e: p1 J% o& L2 I3 w& @1 |
1 O) ~/ M2 Z2 c' Y4 M. T. w1 Q( U" t: s: v: {7 [
. K8 R* u9 J7 e9 J- ?Haematologica. 2011 Aug 9. [Epub ahead of print]) C. H# s" c8 o% x) w! V: @: N/ O
Durable complete molecular remission of chronic myeloid leukemia following' N# N2 c3 D( o Z
dasatinib cessation, despite adverse disease features.
8 k" k% j; F( e2 b6 }9 ORoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.# t, c! ?0 G' k; k; G
Source5 Z y- x4 o0 P, l+ C
Adelaide, Australia;: f/ g7 S, e3 l4 a! p2 R1 X; M
, v9 o6 w% z! \, _3 r6 UAbstract
0 X; ^: k% x0 X, d& |Patients with chronic myeloid leukemia, treated with imatinib, who have a
4 J( [3 s* R1 u1 K3 \" e$ ndurable complete molecular response might remain in CMR after stopping5 W7 {) l. q" D1 t4 c& |: ]
treatment. Previous reports of patients stopping treatment in complete molecular( D+ e6 u! S# s* x+ z1 V
response have included only patients with a good response to imatinib. We' e7 }3 m) d# B% ]8 B( N6 G
describe three patients with stable complete molecular response on dasatinib
& U, O; g' g5 x( Gtreatment following imatinib failure. Two of the three patients remain in
; \1 J( k/ a* B/ J9 m% lcomplete molecular response more than 12 months after stopping dasatinib. In
. A7 S, r& U) o( ~4 R/ j/ G4 ^these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
/ u3 Y: m3 L- c( S% }4 U. }show that the leukemic clone remains detectable, as we have previously shown in
& j6 k( L4 T) U2 ]! @8 aimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
" ~" b$ i1 R$ m# V1 ]the emergence of clonal T cell populations, were observed both in one patient
2 X$ @! b& q+ Q4 e1 p9 a+ L7 vwho relapsed and in one patient in remission. Our results suggest that the' R7 p& u4 x% \
characteristics of complete molecular response on dasatinib treatment may be G* c' j) e3 L+ F; E& I6 L$ j
similar to that achieved with imatinib, at least in patients with adverse
: `- ^6 N+ _# adisease features.$ z* S, I, c! u1 f, k9 f5 b4 Q" y0 m4 k
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