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。3 R: I8 U+ `. }" _+ X. f
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。
2 D; u3 W& G$ X8 W) t! P) }
. f/ Z/ i% K8 @. D3 l作者:来自澳大利亚
, f" c, }* i3 G0 ]来源:Haematologica. 2011.8.9.
0 h6 d% v. w7 BDear Group,+ C t) r/ W D* G1 l: D
! A6 o, F7 n5 q5 J7 P) F, `5 D( ?
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
( o! u- r r$ V' ctherapies. Here is a report from Australia on 3 patients who went off Sprycel) w1 _' r$ ]. n; S" Z
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
" I- C% V% v! m# |! S$ q5 uremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel; m4 v0 `$ s0 u+ T
does spike up the immune system so I hope more reports come out on this issue.; p. \! ]# s2 t" _8 l; l& x1 R- ?
2 x/ Q# W6 C, {0 Y, i" zThe remarkable news about Sprycel cessation is that all 3 patients had failed
) f% h- Y$ J" @; A+ I$ @+ M XGleevec and Sprycel was their second TKI so they had resistant disease. This is. \5 y1 F8 p, c' [
different from the stopping Gleevec trial in France which only targets patients
8 T" J- Q& _# q/ \/ j& f6 Kwho have done well on Gleevec.2 f$ J( d* E& k: f+ Y- f
; z) d' T6 t5 j+ _- b; `1 i7 ~# MHopefully, the doctors will report on a larger study and long-term to see if the( s7 G4 b! @4 p$ k1 H1 {' F
response off Sprycel is sustained.: B4 w6 W, }5 \5 W" R J& |
; Z; L/ u; |! Z& o, |6 ~Best Wishes,
; }: l: H. o5 `3 m; UAnjana% }4 O& z: F6 j
' `& {6 w9 b! o, R
3 ~: g, W9 X& E9 s2 f5 t
2 e2 S3 Q) u, m) j \
Haematologica. 2011 Aug 9. [Epub ahead of print]* w4 @ k6 N5 H9 E6 `2 I
Durable complete molecular remission of chronic myeloid leukemia following
$ A K& H% N% A4 p! Tdasatinib cessation, despite adverse disease features.
7 l. O8 g5 F2 H f% ]Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
& V8 p) Y/ \1 u* _" kSource; L0 l* B8 J" f" |$ r
Adelaide, Australia;: L4 }0 q. O8 E
4 C; j/ j- v Y m8 P# P( f
Abstract5 T. G2 E4 `" W w5 L
Patients with chronic myeloid leukemia, treated with imatinib, who have a
( J+ q% B# K$ ^( q. H1 ?durable complete molecular response might remain in CMR after stopping& x# p; d% _( J8 B5 |+ H3 v8 F% W
treatment. Previous reports of patients stopping treatment in complete molecular+ H' H* l7 k+ Q
response have included only patients with a good response to imatinib. We
) X c1 Q1 r& V ?- N2 ndescribe three patients with stable complete molecular response on dasatinib: ~6 M9 R- V; ?8 D: q: U# Z7 s
treatment following imatinib failure. Two of the three patients remain in1 F6 D7 [" C) m! S6 b
complete molecular response more than 12 months after stopping dasatinib. In
6 }. n w, n" r( T2 Y" nthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to9 Q4 W' }- @$ a* O2 ~9 U; V ?0 z3 Y6 U
show that the leukemic clone remains detectable, as we have previously shown in% T* \5 H/ r6 M- f* [
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as9 T/ `: @- N% ~9 k( G
the emergence of clonal T cell populations, were observed both in one patient" |" e9 B9 `! d! |
who relapsed and in one patient in remission. Our results suggest that the* ]) s) i- b; q# d. B
characteristics of complete molecular response on dasatinib treatment may be- x; d) @8 ~ t; z& M
similar to that achieved with imatinib, at least in patients with adverse# A: n" m1 x- |+ o
disease features.
9 P4 s/ x! A* c& G8 o |