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。
& x9 w1 M7 a% v: m3 F7 a. J& F 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。1 K. g1 _ N3 M& u3 f2 c2 U4 @+ n! P
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作者:来自澳大利亚
5 j Q5 s$ ]' y5 a1 @/ a* Q来源:Haematologica. 2011.8.9.
# W# n6 S( L& e/ _0 K* g3 RDear Group,
+ `) I$ m* N1 R! B& f0 d% ~' O
: a# E. w0 j8 {) l/ hSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML, v! e8 T! ~* Q% h
therapies. Here is a report from Australia on 3 patients who went off Sprycel/ R6 T0 i* J7 [/ H& q
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients% b/ i: k7 H: r* R! K6 w. c- ?
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel% F7 G: D& i3 {( q/ U( x
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 failed
; t r9 J( n- r. K8 i k) MGleevec and Sprycel was their second TKI so they had resistant disease. This is
' ]% A4 W* A i. U+ n5 Zdifferent from the stopping Gleevec trial in France which only targets patients+ j, p+ g5 K# C3 b1 i1 h# Z
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
# b4 R$ y. ]8 R presponse off Sprycel is sustained.
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Best Wishes,
& m/ Q) F6 ^1 l" j2 E. |Anjana" W6 ]8 C4 D8 e2 |3 y/ v( y' ?; }+ m
2 a5 b( o+ a' F" M) h: n9 r1 O! s) x
+ W+ U# S0 j7 X3 h
' W4 y2 s$ P# F. ?# J2 e% q# OHaematologica. 2011 Aug 9. [Epub ahead of print]
( b: |: Q, f4 g) D5 {1 r: a, t. |Durable complete molecular remission of chronic myeloid leukemia following
* w7 }1 t3 [0 g/ Ndasatinib cessation, despite adverse disease features.3 k, h2 K. ?9 Z2 I
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.7 m0 X: n9 d; F2 r5 S1 i6 ^! U
Source7 p% j, [( e$ r2 `
Adelaide, Australia;. ?5 K* [2 l# Q, q
8 @. `$ [9 C" t" ^7 WAbstract7 V0 G( ~ H; s6 L, ?, I, h
Patients with chronic myeloid leukemia, treated with imatinib, who have a. W4 |% E) v1 Z" D( n
durable complete molecular response might remain in CMR after stopping1 U+ d1 ^8 [9 y! A
treatment. Previous reports of patients stopping treatment in complete molecular4 H& q J1 E! v" d% R8 ^
response have included only patients with a good response to imatinib. We8 w" @( Z a( y0 m
describe three patients with stable complete molecular response on dasatinib
. o V4 P- r4 ~/ atreatment following imatinib failure. Two of the three patients remain in
: B! K# _: C z+ m1 K& ycomplete molecular response more than 12 months after stopping dasatinib. In, o/ e! v' e* T0 Y) s
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to$ l* S1 q; p1 \. D
show that the leukemic clone remains detectable, as we have previously shown in
: W$ ~: @$ K$ S2 vimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
9 t( s! ?( U7 [; }& j3 tthe emergence of clonal T cell populations, were observed both in one patient
+ R0 b7 a1 @$ o9 wwho relapsed and in one patient in remission. Our results suggest that the
1 i$ _3 ~2 \4 K- g+ Hcharacteristics of complete molecular response on dasatinib treatment may be
3 S8 o8 g T' {+ nsimilar to that achieved with imatinib, at least in patients with adverse7 k9 z& e5 y$ ] w
disease features.
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