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。
+ F* `* l$ ?0 v8 K 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。
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作者:来自澳大利亚
; w' _0 C6 r7 q9 {) y来源:Haematologica. 2011.8.9.3 K8 O, Q5 D8 O3 v# t
Dear Group,3 Z# m5 t' Q9 K0 W
3 v4 k) {) z* ^% e; USome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
* w- Q S. D6 p# W W8 b! Ltherapies. Here is a report from Australia on 3 patients who went off Sprycel# s+ w' u2 d+ O' t. e) e
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients A8 H6 G- {* ~$ G: ?
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
" k1 y% K. l5 I/ q# udoes spike up the immune system so I hope more reports come out on this issue.
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! a9 e/ R& M1 X) u4 [9 d( LThe remarkable news about Sprycel cessation is that all 3 patients had failed8 J1 g8 K& U ?" o6 n! \" V& e; S
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
1 c$ b4 R' `% sdifferent from the stopping Gleevec trial in France which only targets patients! |6 J8 L6 S1 |: Z8 E8 ^
who have done well on Gleevec.' Z K/ j D- U! w8 ] n
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Hopefully, the doctors will report on a larger study and long-term to see if the9 q6 L/ u: {( y$ ?8 Y9 ^. s
response off Sprycel is sustained.
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2 h% k* } s; F; hBest Wishes,% f* n# `4 j; S# M4 j7 h: z/ M, Z
Anjana
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/ g1 F" b. R1 v4 nHaematologica. 2011 Aug 9. [Epub ahead of print]
: P2 W1 e6 o- {8 R1 ?4 }+ ]Durable complete molecular remission of chronic myeloid leukemia following
/ ]2 D# y2 s9 V3 Idasatinib cessation, despite adverse disease features.& C" e* T/ N4 S' }6 r- o5 ~
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.. N( i6 Y; h1 X/ Z
Source
. g+ i* I) D! l- R4 {$ e$ aAdelaide, Australia;
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Abstract) Z O8 q' p, z {! {, W) ~- U
Patients with chronic myeloid leukemia, treated with imatinib, who have a
. C A& N8 @" s4 Z" a( cdurable complete molecular response might remain in CMR after stopping
2 ~& i+ L k6 S& q* B0 Atreatment. Previous reports of patients stopping treatment in complete molecular
* N+ ?/ ?! [' P8 r( [; }" X- F$ k7 z! Fresponse have included only patients with a good response to imatinib. We1 K3 {% o7 H) F
describe three patients with stable complete molecular response on dasatinib
$ i+ Y9 q. ?, E7 Itreatment following imatinib failure. Two of the three patients remain in" |; Z" T4 {5 u2 Y: h+ s {3 o
complete molecular response more than 12 months after stopping dasatinib. In2 t# B4 `7 {$ J% O4 l8 g3 J2 `4 p
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) U# n3 }0 g1 B" q P* H; Lshow that the leukemic clone remains detectable, as we have previously shown in6 O8 Y& u( L7 c. u/ A) J5 x
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as E( y) d$ b' i2 x' z/ t9 I2 q- x
the emergence of clonal T cell populations, were observed both in one patient
( Q) b4 i$ ]5 qwho relapsed and in one patient in remission. Our results suggest that the
7 u f. X2 |1 h8 @+ @3 ^- v" Tcharacteristics of complete molecular response on dasatinib treatment may be5 L% ]; |/ H# X' N1 C
similar to that achieved with imatinib, at least in patients with adverse4 P) v' P9 b( ^# q3 I" p
disease features.* c7 s6 {% ^; e7 J5 ?2 b( g2 q& I5 Y
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