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。$ b( s* Z4 Z/ U: v" m; b. R
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。5 ]+ x/ N) s' b J7 G/ v: C6 I
7 Z0 ^& P! V7 |+ Z5 o: ~2 U作者：来自澳大利亚
+ W" V) b" z$ U! S" {0 {; ~来源：Haematologica. 2011.8.9.
1 t) Q5 @: y* W' d; v9 s4 Y/ YDear Group,. H! k3 p8 ?1 E8 R2 c. P8 m$ a
0 R: g8 z9 F- W' e. S' C, t6 A7 ~
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
; \, G$ g3 u, H `6 J, A Utherapies. Here is a report from Australia on 3 patients who went off Sprycel" c# a3 E& h) G: Q% K; m
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
+ O4 j& b& z) w! Y0 j& xremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( c# z! [1 H" P- M" K# M- `/ D
does spike up the immune system so I hope more reports come out on this issue.
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+ P) z: K0 s* v v. }1 ~$ E6 tThe remarkable news about Sprycel cessation is that all 3 patients had failed
3 H* S& j3 u. p2 m4 mGleevec and Sprycel was their second TKI so they had resistant disease. This is
+ K# m, t& H3 K0 o* f3 y# ]different from the stopping Gleevec trial in France which only targets patients8 Y5 N/ d. ?5 h1 X7 K: S8 G* P
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the: T6 \1 y4 O0 k
response off Sprycel is sustained.! O% T8 K( m3 g8 i" h
) u9 |7 A$ G v* }& g0 ^& D6 sBest Wishes,& C2 t4 c( W& e- u7 A
Anjana
7 v3 T4 s/ P4 }$ P: n) d; o9 A) m) O- k* a4 N0 p* h) B* ]9 Q; L
9 l* z% L* c1 F5 `2 o( T6 A( ]
u5 S' _" E: tHaematologica. 2011 Aug 9. [Epub ahead of print]5 j$ z$ k% _2 X8 z$ K
Durable complete molecular remission of chronic myeloid leukemia following+ ]1 A9 v. h6 M6 O" B
dasatinib cessation, despite adverse disease features.
; a$ W1 J: R- m) IRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
4 p. g6 Y# A) W; {2 aSource
4 j' C, w0 a5 ^; u0 G) G/ k( m$ kAdelaide, Australia;
7 I! c6 ?: t4 Z @# J0 c4 b( v7 E2 ]$ t! a2 G( A0 W
Abstract9 e5 _, v7 i0 j$ D1 {
Patients with chronic myeloid leukemia, treated with imatinib, who have a
! g2 ]$ w. L p$ p% ?/ fdurable complete molecular response might remain in CMR after stopping
, }' E0 \: N4 u) M) t) Z, q$ A& _treatment. Previous reports of patients stopping treatment in complete molecular* b) U/ v# r* k4 F: }
response have included only patients with a good response to imatinib. We
9 l. f; d _/ d' t5 }0 L8 V3 Rdescribe three patients with stable complete molecular response on dasatinib( ~+ S0 C9 D8 f% p
treatment following imatinib failure. Two of the three patients remain in( `+ J8 l# a" Y9 y1 o
complete molecular response more than 12 months after stopping dasatinib. In
. @9 v4 o" {# B4 o" p6 cthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
. }$ L8 _ Y1 F- _# Eshow that the leukemic clone remains detectable, as we have previously shown in
; h* l/ u# x" K( I/ f6 Z: gimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 ]# Z# y; R9 k+ M/ [9 ]the emergence of clonal T cell populations, were observed both in one patient
% Z" O" B: b" G. [; L9 G4 R+ q, gwho relapsed and in one patient in remission. Our results suggest that the; U9 q; F3 q8 [, k! V5 E
characteristics of complete molecular response on dasatinib treatment may be
/ C0 {+ J" H" T4 T4 z$ y2 s* j7 vsimilar to that achieved with imatinib, at least in patients with adverse2 L; H. ~$ W6 Q9 \0 i
disease features.
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