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。
$ Y8 C+ f( k7 q' V1 f8 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。
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4 y: R# d ]/ ?, x9 u" G作者:来自澳大利亚
5 O0 T, Y7 R" C) S4 ?来源:Haematologica. 2011.8.9.
- {9 V- F+ f+ p% ~: v- g9 U" Z/ iDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
) N0 T! J- `/ I. K) `3 Ztherapies. Here is a report from Australia on 3 patients who went off Sprycel& R9 d' G$ h1 }7 h; h [
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients9 D* O% X! I/ x6 t4 n8 s7 ~
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel2 n ~' Y% J* V8 C
does spike up the immune system so I hope more reports come out on this issue.* K9 h: V3 s9 b$ X
1 |( N% `9 Y- wThe remarkable news about Sprycel cessation is that all 3 patients had failed
7 Y) \9 S' _4 X* z( M* EGleevec and Sprycel was their second TKI so they had resistant disease. This is
- F: E* c# l _# U% c2 Odifferent from the stopping Gleevec trial in France which only targets patients+ p7 @ s! ~: t4 |
who have done well on Gleevec.( D5 D' S# p. }8 z0 C) Y+ J! O
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Hopefully, the doctors will report on a larger study and long-term to see if the
, T4 o7 N& x; o3 O9 a! L+ Zresponse off Sprycel is sustained./ F9 Y1 V a0 b
2 h2 j0 Z# m- c2 u$ VBest Wishes,
; y" ~2 l8 p9 }1 H, ]: e% p6 j4 hAnjana
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, @2 D! e$ B! x3 AHaematologica. 2011 Aug 9. [Epub ahead of print]2 g9 R) @. |1 P" ^$ f" X, w. \" j
Durable complete molecular remission of chronic myeloid leukemia following
6 ^8 s# Q$ H1 D, d! Odasatinib cessation, despite adverse disease features.$ v0 W8 Z6 O/ I% N" a3 r& \" W
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;4 \% T4 w: c- I/ d( D: d4 ]7 K
4 ]* T! t0 E5 C. o% nAbstract
" j4 @& m9 V) Y6 D+ jPatients with chronic myeloid leukemia, treated with imatinib, who have a$ C! s3 v1 v. D I+ u$ t
durable complete molecular response might remain in CMR after stopping
5 E4 `4 Q* C6 u/ v5 m3 ^treatment. Previous reports of patients stopping treatment in complete molecular
( I+ ^& K! P' ]+ @: \) wresponse have included only patients with a good response to imatinib. We* B# ^# ^4 u& H* g3 G K
describe three patients with stable complete molecular response on dasatinib( W; \( w& }; x( O
treatment following imatinib failure. Two of the three patients remain in
( _! _! v, L- d: f8 ?, ]1 u) hcomplete molecular response more than 12 months after stopping dasatinib. In
6 u. N. n4 n' b" W" K7 @these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
3 s2 B, ]( S0 @show that the leukemic clone remains detectable, as we have previously shown in$ P( e; B2 m$ Z; A* B- A+ e, ^
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as) O$ x! W( o. x2 G# u
the emergence of clonal T cell populations, were observed both in one patient
& s9 T4 k! `9 \. Q( O; Bwho relapsed and in one patient in remission. Our results suggest that the
# d Y3 X' [0 W8 l$ h3 Ucharacteristics of complete molecular response on dasatinib treatment may be
% `% V4 \1 `( k: V7 Bsimilar to that achieved with imatinib, at least in patients with adverse; S6 C" h% q; m" C/ s( e: l
disease features." Q7 m3 Q/ Q3 L4 J9 x8 P
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