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。
" _4 ?- u$ n- N8 q, f% W# _ 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。& i0 d. u) O1 J0 s; H
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作者:来自澳大利亚
* g5 F# N5 N& v0 W% S来源:Haematologica. 2011.8.9.
" b6 g: r d" zDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML' @$ y6 g9 t1 @+ m8 v5 ~
therapies. Here is a report from Australia on 3 patients who went off Sprycel
# |' \. k: |8 \after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients, R! U3 a! I( \) I, \4 g7 H
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' M# s, Q8 a7 ]: @! N' H: i# N: M
does spike up the immune system so I hope more reports come out on this issue.
3 r) o8 R$ ^7 ~7 D" X- F: W
' N9 g* P% M6 W- S& {/ e& ^The remarkable news about Sprycel cessation is that all 3 patients had failed
$ i9 ^7 \ c/ }% J3 w5 d& f$ h7 O. EGleevec and Sprycel was their second TKI so they had resistant disease. This is
4 [$ k. A4 W; i7 Y) {7 D! J% X2 Rdifferent from the stopping Gleevec trial in France which only targets patients" r- y" U: c+ J! s. e3 ~, b
who have done well on Gleevec.4 Z' x! o% L% G9 G1 }0 @4 Y j! a
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Hopefully, the doctors will report on a larger study and long-term to see if the
* |6 Z9 [+ S7 h- L$ oresponse off Sprycel is sustained.
" I+ }* {! J# `# Z
0 x$ W |/ T, Y. J- U+ G& h$ v3 KBest Wishes,
1 ^$ Z# _- f5 EAnjana8 H7 P8 X/ {' t m
0 V2 K, _* H, z: [) s0 N# M, Q. P4 G) j; N
6 V- m7 P/ d, b6 K% e( n* wHaematologica. 2011 Aug 9. [Epub ahead of print]/ q" A$ ~: Z& L( S: A7 E
Durable complete molecular remission of chronic myeloid leukemia following) ^* m- ?7 ^& R4 S$ @( a
dasatinib cessation, despite adverse disease features.) o: M, ^! |0 a1 d6 S, z
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.: k+ m# A% J8 }. X$ U4 o
Source
+ ^8 w: t" m: q- J. FAdelaide, Australia;
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Abstract
9 I" B/ b9 f4 P: zPatients with chronic myeloid leukemia, treated with imatinib, who have a3 ?: C: j. F- A: I- {, {" s7 k
durable complete molecular response might remain in CMR after stopping
# m+ X% C/ }& Y n G$ M9 Ttreatment. Previous reports of patients stopping treatment in complete molecular- y: _5 r7 U/ a3 y1 M, M
response have included only patients with a good response to imatinib. We1 |) I% a# |! Y6 |* y
describe three patients with stable complete molecular response on dasatinib8 Z/ ^; P$ C& R) E0 V& y1 j
treatment following imatinib failure. Two of the three patients remain in
) l- j8 w7 z8 _% d3 W4 ~1 u6 A! m: Ocomplete molecular response more than 12 months after stopping dasatinib. In( H( z+ K" Z5 O* s1 E, i. \
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 l6 S. p. p" i0 X4 ^1 |
show that the leukemic clone remains detectable, as we have previously shown in
* \8 {0 V7 Q- y; |8 u yimatinib-treated patients. Dasatinib-associated immunological phenomena, such as8 q+ W% F: r$ r
the emergence of clonal T cell populations, were observed both in one patient' e5 i) Q( J. a
who relapsed and in one patient in remission. Our results suggest that the! L& l+ n0 }6 D& ?: F8 \3 y
characteristics of complete molecular response on dasatinib treatment may be
3 J4 \8 K+ [, M Z# Jsimilar to that achieved with imatinib, at least in patients with adverse. ?5 I2 e* @5 s7 v
disease features.0 P x4 g1 [- {* W( K7 Z5 I1 b) A9 }
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