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。. J/ {6 _2 B! F7 K2 l4 T# L
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。! @0 W, W. r9 Z' X: A
- c! m; f2 H, |2 ]. S作者:来自澳大利亚
8 d& }: M& T& A' N/ z5 Z& g9 g来源:Haematologica. 2011.8.9.% W; U" L- D. [& E. ~
Dear Group,( v4 C( U7 E3 K) L
* o( q2 T% r0 N( j+ W5 p, L0 H# [& w
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
* t4 N8 H7 `; X/ v3 v% m7 |therapies. Here is a report from Australia on 3 patients who went off Sprycel# o* u3 L* Q( l* ~; h9 Z% U j0 @) E; Y
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
# ]3 K. B) ~4 U+ v/ B0 Wremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 R: s6 o5 i# `! D8 ^6 D( }, h
does spike up the immune system so I hope more reports come out on this issue.
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' F1 w5 ?; l! ~. e4 Q& B+ xThe remarkable news about Sprycel cessation is that all 3 patients had failed3 \4 X& h9 }" g+ t4 I- z! K
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
1 r2 N2 s: q6 C1 D* \/ Gdifferent from the stopping Gleevec trial in France which only targets patients9 o+ n3 R5 ?+ o/ s) C
who have done well on Gleevec.! J# w d9 j5 i( \0 T. N: a
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Hopefully, the doctors will report on a larger study and long-term to see if the
: ^* \/ g9 a* `! c% N) K3 T! xresponse off Sprycel is sustained.
) O! h- ~1 \. J* s
$ j P8 N, b5 tBest Wishes,
' u z3 f0 t$ \& t* AAnjana$ B# i) x1 T( h
: M! ~7 F# F8 g, t+ Z/ g4 Q E w0 j2 E3 X5 U
! w4 N g% t1 hHaematologica. 2011 Aug 9. [Epub ahead of print]
; O; z& s0 p" Y' o9 ?- T& XDurable complete molecular remission of chronic myeloid leukemia following3 n9 P8 ~5 H6 ~& o% ^. ^
dasatinib cessation, despite adverse disease features.
6 b7 \ S# Q. v2 J4 wRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.* o6 N& N4 |9 k7 c+ b
Source) s, B) R' y5 V# t# \: S; Q
Adelaide, Australia;8 D* }" g( q" V2 _
" n5 b: ]: _! y7 `8 B6 B
Abstract
' ^$ l1 k) @( R3 S. pPatients with chronic myeloid leukemia, treated with imatinib, who have a6 F# ^4 q- q4 ~/ U: w5 {
durable complete molecular response might remain in CMR after stopping
: r8 ] ~0 A! [3 A" R2 _treatment. Previous reports of patients stopping treatment in complete molecular2 k8 ]4 j9 k; v7 _- L U+ K+ a, ?3 ~0 e% Q
response have included only patients with a good response to imatinib. We
! T- C, Z" x( L9 p6 T6 C3 N) {* Cdescribe three patients with stable complete molecular response on dasatinib
7 L4 }% U' _3 {# R1 u+ ftreatment following imatinib failure. Two of the three patients remain in6 \" T' x; _' w; i/ v
complete molecular response more than 12 months after stopping dasatinib. In
0 { Z6 E2 g9 Ithese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to. J" i/ i" _7 J o( j3 I
show that the leukemic clone remains detectable, as we have previously shown in( t$ }" T! z, q$ j) O7 l/ Z
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 _3 A8 c; g5 m1 s* c; _the emergence of clonal T cell populations, were observed both in one patient$ d# C. W" t: U
who relapsed and in one patient in remission. Our results suggest that the+ g2 _8 d5 ?% N8 Z: i
characteristics of complete molecular response on dasatinib treatment may be% C. ?/ E+ w9 I; g4 j
similar to that achieved with imatinib, at least in patients with adverse$ [' b( p2 S# [0 R3 M
disease features.- D4 h5 [6 G& c! p4 J
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