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。
" U. D( q* H& J. Q6 K) l: z: ?6 v. M 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。. O1 a) K& K* \) Y8 Z) c
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作者:来自澳大利亚
$ G" d i0 C6 e g来源:Haematologica. 2011.8.9.
; a6 ], D2 y5 l" ?4 w( S' YDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML, ?1 ]) R. |$ t+ c- M5 `) J' R" o
therapies. Here is a report from Australia on 3 patients who went off Sprycel
4 {% b* `; D B, n5 Q) ?3 o4 cafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
' O: }" D% X$ D j" z) Lremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
, A& L3 F F: ?! K6 L adoes 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# @2 P% N9 ~2 c7 t1 I
Gleevec and Sprycel was their second TKI so they had resistant disease. This is5 n# k! y, o: \3 `
different from the stopping Gleevec trial in France which only targets patients
; r5 Z- r- b" x6 qwho have done well on Gleevec.1 k+ v4 d. r# J
4 ]! N0 ^& v! D W# NHopefully, the doctors will report on a larger study and long-term to see if the
3 o7 E+ h4 o4 L c! lresponse off Sprycel is sustained.; W' A, F7 a% C* f2 H. m$ E4 w
) i z1 @, \; G1 y* HBest Wishes,( M9 w9 f4 @# ~# [! ^
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]6 L- t0 ]# Z y3 R. t
Durable complete molecular remission of chronic myeloid leukemia following5 Y. t- V& ]0 T! c
dasatinib cessation, despite adverse disease features.
/ k# G/ j9 M9 ] M& N: h# F1 x1 VRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
8 W; P) M. \) B. |Source
$ N( h, q" H0 i9 WAdelaide, Australia;; S( S: N2 i7 T/ |2 t2 i
0 B! l' S2 W8 v( j+ A7 nAbstract
# I4 [0 S% b+ ]- D; P( VPatients with chronic myeloid leukemia, treated with imatinib, who have a
% P* Z. G; w" c/ l3 g: Qdurable complete molecular response might remain in CMR after stopping6 |! g, ~. P$ }
treatment. Previous reports of patients stopping treatment in complete molecular
5 \2 ?$ o4 D z1 o% u/ k# lresponse have included only patients with a good response to imatinib. We- F! u. X' c, ^2 a2 W+ O6 O! d% S
describe three patients with stable complete molecular response on dasatinib, _6 P4 |6 s9 b- f# o
treatment following imatinib failure. Two of the three patients remain in6 p% K% x- ^( Y! l
complete molecular response more than 12 months after stopping dasatinib. In5 V( L& z; z( v: o
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) b0 R. G d( o! _% ~6 [5 Ishow that the leukemic clone remains detectable, as we have previously shown in1 p7 i) w* q) d7 v
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as9 @7 `) I n1 H+ }+ H- P0 U
the emergence of clonal T cell populations, were observed both in one patient
1 J% P' }5 I0 ^: K7 s$ S2 U: R$ fwho relapsed and in one patient in remission. Our results suggest that the2 ^- i# N0 v+ m% ^* v
characteristics of complete molecular response on dasatinib treatment may be
+ `- I8 n3 p6 C, s& |9 x# Csimilar to that achieved with imatinib, at least in patients with adverse- @! [, d& p7 g* @/ G
disease features. o u7 N9 W0 C, ^2 C7 a$ _" d0 \
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