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。- r6 W; F( ] i7 G) O
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。/ ~: `1 D/ X5 I* g" V
* f/ w; z% `) ?- R, f1 @作者:来自澳大利亚# E2 j4 C8 Z1 @/ a [
来源:Haematologica. 2011.8.9.: r, F- y" n: m |! B; X* o
Dear Group,: i0 F" I0 S2 p! n
& H/ e5 j; g5 W& W$ g+ QSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML( k V+ x3 D5 z- q/ |% G
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 e& D2 J; v# `7 A/ q
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
3 S2 i) n8 F* ~7 R3 H7 Dremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# k, b' ^! b* i. s! P% ~0 s, V6 \does 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
1 p* @: O9 w# j- ^; K* W2 kGleevec and Sprycel was their second TKI so they had resistant disease. This is
0 F9 x& g; s; h4 g$ ^different from the stopping Gleevec trial in France which only targets patients; p# ~ C1 R0 K$ F8 b/ m1 S
who have done well on Gleevec.8 Y* J( R. ^' r4 U
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Hopefully, the doctors will report on a larger study and long-term to see if the W. E- A# P+ s! |& q
response off Sprycel is sustained.9 F5 P- f1 W# c1 u. A
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Best Wishes,
1 r. K% O7 ?( w I' |# B5 a, ]* }Anjana
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$ a- r7 E) z# e0 e2 B. _/ H8 i# w. {( p: l) d- ]& V; c* T% v
. r& `4 B% t+ V/ Z) ]1 s; GHaematologica. 2011 Aug 9. [Epub ahead of print]
) R Y# F& ~9 m# \! u7 c* ?Durable complete molecular remission of chronic myeloid leukemia following7 x. \9 x, t# n; m# F n
dasatinib cessation, despite adverse disease features.
5 a& V9 `2 V0 }Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.4 q5 \( S" h+ [% j: s
Source
2 p1 Q3 n9 L& f' q" bAdelaide, Australia;) C+ h$ |, ~6 B7 F+ C; `3 y
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Abstract
8 p4 X0 o0 q% L3 oPatients with chronic myeloid leukemia, treated with imatinib, who have a( ^8 L1 M( P: b6 q- {. U- Y
durable complete molecular response might remain in CMR after stopping( L. a; e9 Z: P7 c* k& J1 x; ?6 H
treatment. Previous reports of patients stopping treatment in complete molecular
3 O% i& U2 W7 ]9 l3 r U9 u+ |response have included only patients with a good response to imatinib. We
- Q6 ?. @& A, c0 p" rdescribe three patients with stable complete molecular response on dasatinib/ Y1 U5 A2 I- P. J: W
treatment following imatinib failure. Two of the three patients remain in$ c& M1 Q9 T. U! K
complete molecular response more than 12 months after stopping dasatinib. In
/ o+ R8 b, z" c o4 _8 N" h) fthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to9 {2 [1 E+ Q, p+ A t
show that the leukemic clone remains detectable, as we have previously shown in( u' R: p4 c y0 Q# q) H& {2 I t
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 I0 ~* T) t1 V* e3 L2 Y9 U
the emergence of clonal T cell populations, were observed both in one patient
1 u; g+ a' _5 w/ P/ q' Zwho relapsed and in one patient in remission. Our results suggest that the3 b; n( f! u# a3 g) O
characteristics of complete molecular response on dasatinib treatment may be y- e! }6 x1 z$ D
similar to that achieved with imatinib, at least in patients with adverse! A9 `6 ~, p6 |9 P" s. \8 E
disease features.
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