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。' Q. [" d6 d( t! w1 H$ g. ]+ h
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。3 m, ]0 S3 k7 k; [
, F7 O, Y4 V3 N. \( J) r9 p' _
作者:来自澳大利亚
% M& N6 C( ?2 U) i0 Q0 B& s9 v来源:Haematologica. 2011.8.9.: _! u! i; W& k7 o6 _/ p
Dear Group,
" U7 L$ D# h9 p; N. V1 o, o
: _" |0 c/ ]4 Q* p0 @Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
- S$ S5 s3 M6 \4 Ktherapies. Here is a report from Australia on 3 patients who went off Sprycel
* B9 R6 i5 k% u; s2 Q, b8 Zafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients) F( P+ W3 H( @9 W# m$ V
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. C) c# T/ v3 J7 ]6 v
does spike up the immune system so I hope more reports come out on this issue.* Q# G5 P- ?. R
- n- m& X! N% R& w2 }5 DThe remarkable news about Sprycel cessation is that all 3 patients had failed8 l% q8 c7 A* f' i! W6 W2 q
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
: B0 O T1 K. odifferent from the stopping Gleevec trial in France which only targets patients4 I" Q) V3 H% N0 N( ^4 p
who have done well on Gleevec.
' n% W% i2 V+ g8 y8 K8 n" V$ n9 `0 ~/ q, }
Hopefully, the doctors will report on a larger study and long-term to see if the( w6 E( C: _4 g4 {" q+ [5 B
response off Sprycel is sustained.& R+ S# l. q0 h2 r$ T; Z
/ R) y/ y! W* I8 \$ \
Best Wishes,- @4 J" M1 ]# h6 n* }3 P* Q3 e
Anjana
( _1 l2 g& Y5 N Q M. F" z! p- M' t3 M2 J$ T2 }
) O7 ]4 `- r8 M$ y& y
( O# p1 J# K: T4 [* LHaematologica. 2011 Aug 9. [Epub ahead of print]
( I$ {6 |, h/ P8 T. I5 H0 r, GDurable complete molecular remission of chronic myeloid leukemia following
/ \. O$ g- q3 e* |9 s( ?dasatinib cessation, despite adverse disease features.& j6 ?! B8 S; t* g- Y a( c
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.8 J J* f: n Q; O: h9 X4 E* M
Source0 l" M3 G$ O, m) k. J& y! A) r) R! F( Q
Adelaide, Australia;9 N+ I/ [5 t# o. Q
! P) ] L' i! \5 @" ~% c9 ^% r
Abstract
0 ?' I% X% V2 t3 S8 ~$ V0 r7 BPatients with chronic myeloid leukemia, treated with imatinib, who have a" l. Y7 [+ l; e1 k
durable complete molecular response might remain in CMR after stopping
4 |8 X S3 Z4 l% v8 E4 `" f2 c6 |treatment. Previous reports of patients stopping treatment in complete molecular& v* c8 c$ Q9 Q$ q
response have included only patients with a good response to imatinib. We
6 L# h% I" A* `7 A1 zdescribe three patients with stable complete molecular response on dasatinib
. i- ^2 a) L) e k5 m- m ftreatment following imatinib failure. Two of the three patients remain in8 s: _$ x3 z. W$ z2 C; F
complete molecular response more than 12 months after stopping dasatinib. In+ r; H! t1 ^) I: ~+ \) k6 @- g
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to \4 p' V D9 N; R8 C" \
show that the leukemic clone remains detectable, as we have previously shown in
+ a3 t& c0 f# v) E9 ^imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
3 i; t! z6 f5 {$ b$ jthe emergence of clonal T cell populations, were observed both in one patient; `* Y* ]4 f7 ]* k9 E m
who relapsed and in one patient in remission. Our results suggest that the
0 C3 N( i4 ~& V$ i1 g2 d$ `characteristics of complete molecular response on dasatinib treatment may be
; ^" ?4 U" \ m( ~similar to that achieved with imatinib, at least in patients with adverse$ K$ O7 H1 v7 f
disease features.) r& X; N4 H1 M4 K+ Z, B4 i
|