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。 ^/ C' ?! z0 n
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。6 r$ o' o; [- N1 |
( U8 q( ]+ w! E h作者:来自澳大利亚
8 a5 Z/ X- g% W7 T+ B来源:Haematologica. 2011.8.9.
6 d5 k5 h+ Y+ }3 W% E$ cDear Group,; R. n7 W/ u' B0 _3 {4 ?
9 ~. w0 N! w9 d3 O& w3 x
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 |. E% O+ I2 c5 N0 dtherapies. Here is a report from Australia on 3 patients who went off Sprycel
* n1 O* g* I+ S! _( Vafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients2 \" Q4 \- b% T2 \. z7 H
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
) y% b8 X( M1 {does spike up the immune system so I hope more reports come out on this issue.8 S) ~' v) ^( z# D3 b5 e2 b7 N* F2 }
) S L% o9 h2 Q. ?) bThe remarkable news about Sprycel cessation is that all 3 patients had failed
- E* D9 a4 z! _% T% xGleevec and Sprycel was their second TKI so they had resistant disease. This is
4 I# u! z, V# V ~2 Ddifferent from the stopping Gleevec trial in France which only targets patients( z$ o- j* e) V4 B# C+ v9 z3 O7 e
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
J3 p8 \8 z H/ h1 D$ b) r1 Oresponse off Sprycel is sustained.5 ]; C+ V% y3 _* j; m, ~
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Best Wishes,
4 l5 `% S4 d; L9 ^Anjana
/ ]) C7 ?% k: S0 k- F9 `- v* x: U* @3 @
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Haematologica. 2011 Aug 9. [Epub ahead of print]
V$ F* l; D* b7 d fDurable complete molecular remission of chronic myeloid leukemia following$ _0 U/ ?9 D* Y! V$ W: y" M) q9 W; x; G
dasatinib cessation, despite adverse disease features., ?/ n: a" x, K# h# M
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
3 V6 p% T# ?& V6 ESource
: n1 T8 J7 ~: l7 [Adelaide, Australia;
8 ?4 `" ^. \7 u7 k7 R4 b9 ~. U1 {( B" k0 A- P! H' i0 ?3 j9 n$ a' h. J
Abstract3 r4 l6 v: v! Y1 M: H1 b8 y
Patients with chronic myeloid leukemia, treated with imatinib, who have a
' ?; s! b# z/ |5 s- ~7 udurable complete molecular response might remain in CMR after stopping
" A: T8 i; A. T( @1 n% dtreatment. Previous reports of patients stopping treatment in complete molecular7 G1 A8 q; X `4 \, Q
response have included only patients with a good response to imatinib. We
, m, J& o! y: R+ ?describe three patients with stable complete molecular response on dasatinib
: k \3 d& K! Etreatment following imatinib failure. Two of the three patients remain in
1 K9 s" P+ i; P! R* C1 jcomplete molecular response more than 12 months after stopping dasatinib. In+ b4 |, ^* |& d# G5 X: |
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
+ q9 k4 e% f+ lshow that the leukemic clone remains detectable, as we have previously shown in
0 s6 R' `8 l2 Y: p1 R9 a( y( Wimatinib-treated patients. Dasatinib-associated immunological phenomena, such as2 a W4 L7 Q# `% w: O3 V @" o
the emergence of clonal T cell populations, were observed both in one patient7 f) X& n( C. s$ T
who relapsed and in one patient in remission. Our results suggest that the
9 A+ h/ z( D2 S D# p3 r8 ?- Acharacteristics of complete molecular response on dasatinib treatment may be
% B9 p4 I1 K& ^' p. a, zsimilar to that achieved with imatinib, at least in patients with adverse7 L3 n. @: D- `/ X# q- `
disease features.
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