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。
- a0 Q. o7 `2 @( E' O( O* ^ 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。$ j' P4 s( |& }! g- S% T" t7 j* o
1 O) }& h7 ?9 K; X A, R* _9 j/ w作者:来自澳大利亚- {8 K' Z# f9 E5 W1 x. ?
来源:Haematologica. 2011.8.9.5 V, _% s _6 R( m0 j
Dear Group,
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7 B/ T& t$ U; f+ x$ s; hSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML5 n1 b( F. o9 F$ ~, ^0 U& q8 t
therapies. Here is a report from Australia on 3 patients who went off Sprycel
9 Q. }* w+ ~7 v) w) z: }after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, d6 V+ V9 S3 f t; d, r+ O/ }remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
* ^- F) H6 E* s' U( q- `does spike up the immune system so I hope more reports come out on this issue.7 m: k% k9 Y1 B
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The remarkable news about Sprycel cessation is that all 3 patients had failed
! ^) ?- `" E! nGleevec and Sprycel was their second TKI so they had resistant disease. This is& {, Y) c8 S5 v" P' @" r1 S4 `
different from the stopping Gleevec trial in France which only targets patients
7 X o3 L: \- Wwho have done well on Gleevec.; x2 M8 ~+ ]4 a# {
1 M: J* A# Y" X7 I7 `
Hopefully, the doctors will report on a larger study and long-term to see if the
9 G! U; \" W3 ^9 G' R8 v; @: wresponse off Sprycel is sustained.
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Best Wishes,
3 M5 q, m: g5 A- D' pAnjana
9 V( _6 m% s+ o& ?! N1 _4 W& c2 d1 a3 v8 D
, p9 H% P6 ~( |7 s$ j% T" o& `" d' f4 r. c
# v; C4 A y% Q/ }* E, L- r/ o$ w' pHaematologica. 2011 Aug 9. [Epub ahead of print]
! E; y& R0 f3 w6 lDurable complete molecular remission of chronic myeloid leukemia following
: @; V/ c. B2 N u0 c1 W" Ndasatinib cessation, despite adverse disease features.8 A" H# B& q) x/ f: E, w1 T
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;! U& v, J! n5 I9 Y- ^
7 [, n* w' s4 G, N" mAbstract
# i) ~! @$ [; w h% p: IPatients with chronic myeloid leukemia, treated with imatinib, who have a
6 \7 C! o D: x2 t. `' Cdurable complete molecular response might remain in CMR after stopping
1 X# {4 j8 L5 n" Htreatment. Previous reports of patients stopping treatment in complete molecular @; R- I2 i! [' E
response have included only patients with a good response to imatinib. We4 R( Q2 n# |3 _& E
describe three patients with stable complete molecular response on dasatinib" z2 C$ ~# o! A8 P3 k
treatment following imatinib failure. Two of the three patients remain in
& L& }" Z: p' o8 Z7 [complete molecular response more than 12 months after stopping dasatinib. In: j: S5 M7 L7 O' \, u4 x4 C
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ {2 h l9 [' W8 c+ x+ A8 ^8 M1 e
show that the leukemic clone remains detectable, as we have previously shown in) V, V- B( n) S' R2 b* G) l1 |
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 M3 A1 R) t8 _0 j% j" Z$ m0 x- a5 ~
the emergence of clonal T cell populations, were observed both in one patient) U7 F3 i$ {* @
who relapsed and in one patient in remission. Our results suggest that the1 t0 I( T: p5 Q
characteristics of complete molecular response on dasatinib treatment may be
/ ^" d b& U% r8 R" \0 wsimilar to that achieved with imatinib, at least in patients with adverse7 I' n& ~4 {2 e! l
disease features.0 N5 P3 y$ n7 Y9 a
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