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。8 {0 q8 i7 n7 C4 ?
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。! R4 j% o( b) W, O- v% J H* |
/ u0 @' y: }/ f5 N作者:来自澳大利亚% @2 x2 D0 h g* Z8 }: t6 [
来源:Haematologica. 2011.8.9.- |6 G5 S7 t9 d9 o) d
Dear Group,; V& q$ |! [* \1 s* `% d. H! b
- N! t* y; N0 fSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
; ]) f6 x4 [1 W2 E9 w Ztherapies. Here is a report from Australia on 3 patients who went off Sprycel
6 {: b2 e* I7 U: oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients- k' m# k. ]) b3 O1 V& T5 b% l
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
4 |2 K1 S8 |5 N3 e! S rdoes 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 failed
2 g+ n* X" H0 O) c3 iGleevec and Sprycel was their second TKI so they had resistant disease. This is9 X9 ^7 G7 f! G: x6 t
different from the stopping Gleevec trial in France which only targets patients
: X4 u; ?5 [$ r2 j& Q3 Iwho have done well on Gleevec.6 X) ?/ u( T+ N
, o W# B7 C7 p1 x7 ]
Hopefully, the doctors will report on a larger study and long-term to see if the
+ F0 {& y& o7 U& w- l; Uresponse off Sprycel is sustained.
5 u I3 ?- P. C: E
7 g% E5 D P7 Z1 Y& z' r$ M7 r+ PBest Wishes,
0 ~# o2 V4 M4 }7 s* u$ ~7 c% PAnjana
a, k4 U% V( w3 B
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! \) O3 @. f4 I4 zHaematologica. 2011 Aug 9. [Epub ahead of print]2 k& u6 q0 H9 i8 x; Z
Durable complete molecular remission of chronic myeloid leukemia following
. l1 S6 f; G+ @5 o) s0 b n$ k5 Odasatinib cessation, despite adverse disease features.; s/ d2 O4 \9 A# E
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
1 I* s0 _9 N, l, gSource) ?% B3 ?+ ]8 D$ S# p
Adelaide, Australia;) g9 [/ o" f1 s& G0 W; v8 [
' ~: w, n$ v! K/ CAbstract
V! [4 d. q& u4 i8 U2 CPatients with chronic myeloid leukemia, treated with imatinib, who have a
# F2 }0 d. Z( W+ A1 H8 R. wdurable complete molecular response might remain in CMR after stopping& ?% Y% y2 V* z. c" f( [ |
treatment. Previous reports of patients stopping treatment in complete molecular
# `- d) K6 v! B: f% Oresponse have included only patients with a good response to imatinib. We5 l7 ?7 r9 z1 ]
describe three patients with stable complete molecular response on dasatinib2 K$ n, e* O* n/ s+ F! {. P; M
treatment following imatinib failure. Two of the three patients remain in5 T$ w( u0 B9 c9 T. j6 `+ f! S4 n% w. y
complete molecular response more than 12 months after stopping dasatinib. In2 J( Y( a4 [! N/ T7 r
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 c# x3 d3 y" x0 ^# M9 U
show that the leukemic clone remains detectable, as we have previously shown in
& q9 A' `* v8 @, k- H" w, E& iimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
9 |- h) o* a2 ]! b d/ I, m' nthe emergence of clonal T cell populations, were observed both in one patient8 T; O6 D1 `* w$ P& N# \
who relapsed and in one patient in remission. Our results suggest that the2 D+ a$ R* o' [# W4 d
characteristics of complete molecular response on dasatinib treatment may be
& A! H. f5 n( m4 i) bsimilar to that achieved with imatinib, at least in patients with adverse
4 N' P0 D9 u9 Ydisease features.4 A- K& N0 D, T3 u) a: }" a
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