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。
+ H! G$ g' {- J% R G 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0 G6 _3 F* w! s& A
来源:Haematologica. 2011.8.9.$ b9 w3 X) \( I0 v; i
Dear Group,! Z* y9 k! b4 }8 x- c
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 }% F+ F% L8 l$ ?& n1 [therapies. Here is a report from Australia on 3 patients who went off Sprycel
# n! w6 v7 b7 Z: {2 safter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
v S- E- K/ W. {/ r9 j# s, |% mremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel \# q- v) Q, P/ B
does 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 failed1 }& }) A1 P# ]5 b1 O5 ?
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
" e) d/ {! H R' pdifferent from the stopping Gleevec trial in France which only targets patients
4 O7 x3 a: r) |/ u% W, N, Rwho have done well on Gleevec.. h# @$ M# U, K! `. M8 a" ]/ S1 S
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Hopefully, the doctors will report on a larger study and long-term to see if the5 a* w, i1 V0 o* A, N% Y
response off Sprycel is sustained.
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Best Wishes,
E/ J; K9 D) nAnjana
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: U' l! Q% @3 w# a; i2 ~Haematologica. 2011 Aug 9. [Epub ahead of print]
# u$ E1 ^" g+ Y8 _; `! A" `Durable complete molecular remission of chronic myeloid leukemia following
s8 ]5 a& B' m& h3 adasatinib cessation, despite adverse disease features.9 }$ L& j8 Q* A; D
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.0 P1 W0 j$ a1 W
Source0 w' x- W. x3 H
Adelaide, Australia;( I4 k( `9 R2 K, Y: `7 h
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Abstract) ^# j" I9 l, w X
Patients with chronic myeloid leukemia, treated with imatinib, who have a
# Q% f4 N0 L; S; x' Sdurable complete molecular response might remain in CMR after stopping7 b+ a+ X$ V7 C1 \3 y6 d6 `8 `% b
treatment. Previous reports of patients stopping treatment in complete molecular% ]' p, Q6 p7 y- g `1 _; B
response have included only patients with a good response to imatinib. We) l3 {0 O' Y6 S! d0 U: `
describe three patients with stable complete molecular response on dasatinib) H! ~8 a/ e7 |
treatment following imatinib failure. Two of the three patients remain in
) |. u2 a, G) e- c, u jcomplete molecular response more than 12 months after stopping dasatinib. In
( A) t ?3 `: k. l7 C% vthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 D9 r7 y- q3 q3 q% b' _
show that the leukemic clone remains detectable, as we have previously shown in( w/ [. v9 [2 }/ s% O
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as7 C* V' C- }0 N$ {
the emergence of clonal T cell populations, were observed both in one patient' Z% m+ C2 h0 v2 F; w
who relapsed and in one patient in remission. Our results suggest that the
0 V" \. p4 |0 p: n. t. Acharacteristics of complete molecular response on dasatinib treatment may be+ I1 ~ d2 t* ^; @: [( \; J
similar to that achieved with imatinib, at least in patients with adverse) y8 t) P3 M4 l. E- I
disease features.
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