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。+ ^+ G" w1 y# @" O5 {( `: g7 ]0 a
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。" E6 O3 e8 X* z8 F2 ]! x
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作者:来自澳大利亚
3 D) g# V- N+ Z) K/ D3 j( Q7 \) b来源:Haematologica. 2011.8.9.
6 w( _$ E4 U" }, k6 z: dDear Group,2 z+ E' I! h4 b6 Q4 C0 V$ J
8 Y! G1 @, s0 V+ R# w2 Z/ K( dSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML1 l1 F/ I1 M2 K& h
therapies. Here is a report from Australia on 3 patients who went off Sprycel
7 @8 N3 s% N+ \/ p( R4 cafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
% X2 h3 L& ?9 X' A6 z* Mremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' Q( u2 O- y9 T! {% t% ?, z& i
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* K) R# X3 s. N/ | ?& _/ ^
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
$ k$ @7 s$ C7 V' U; h) odifferent from the stopping Gleevec trial in France which only targets patients; z% z6 L0 e% T" i
who have done well on Gleevec.9 Y! f+ |1 I8 Q' k5 M3 U, q
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Hopefully, the doctors will report on a larger study and long-term to see if the
- b" Y" k4 Z0 _" F/ x4 w% ]' G, Oresponse off Sprycel is sustained.
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* X9 ` z. b: k6 `) A0 d5 { S2 zBest Wishes,
1 ?$ w3 V, |8 n& V( FAnjana
8 T# Z0 s& S8 `$ b0 Q% s- k- P, C" o8 o' w/ | K% o2 x
. P9 ?/ {1 L+ W) s$ P& H/ K1 h2 h7 c
3 \0 I& b& I: L3 H" W% hHaematologica. 2011 Aug 9. [Epub ahead of print]. [# M# U; \3 v+ b2 ?; ]! \( s
Durable complete molecular remission of chronic myeloid leukemia following: a/ L F, U) ?4 Q* c: w
dasatinib cessation, despite adverse disease features.
$ `9 J1 o8 p3 m" H }Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
$ Z. t$ w t6 @7 gSource& ~3 x- [1 X; |4 P( X) m7 e
Adelaide, Australia;7 b0 Z1 d, J! u1 U; N( o6 ?/ i
3 l( T7 b: U' t7 h3 z1 J
Abstract% f, ~- z+ `0 r7 H& c* Y
Patients with chronic myeloid leukemia, treated with imatinib, who have a/ |4 r" M" A4 x/ n! h' Q
durable complete molecular response might remain in CMR after stopping8 _# Q* O+ d! a" Y& k* `9 C
treatment. Previous reports of patients stopping treatment in complete molecular
; E% E) ^/ e* M) Lresponse have included only patients with a good response to imatinib. We a* G, z8 {! |5 k9 ?. \- K
describe three patients with stable complete molecular response on dasatinib
1 D; W- h/ Y' z2 g# |treatment following imatinib failure. Two of the three patients remain in9 @# h3 f3 ~2 {1 K5 [' g0 O6 x2 a' ]
complete molecular response more than 12 months after stopping dasatinib. In. m, y: ]# V8 I4 A" Y* `- ~
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to4 J: J' ~; x/ c: r8 ?& {* O( E% }
show that the leukemic clone remains detectable, as we have previously shown in
( s" V3 S; D& q, f: a0 Z( T5 Pimatinib-treated patients. Dasatinib-associated immunological phenomena, such as, }, t9 \0 J8 H% C2 `1 |% i
the emergence of clonal T cell populations, were observed both in one patient7 D; ~$ v( q0 l+ e/ ~: a
who relapsed and in one patient in remission. Our results suggest that the% A' Y ^" J' J1 t6 `4 j8 ]0 O
characteristics of complete molecular response on dasatinib treatment may be3 C- p% b: V; ~# F
similar to that achieved with imatinib, at least in patients with adverse
( v6 A. P( g; f0 }; h- Adisease features.
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