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。4 l, V( B$ C1 y# r
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) t4 n! p2 \# j# c6 x% s0 M
来源:Haematologica. 2011.8.9.
* V, Q% _' T8 G# g/ F6 Z0 Q1 KDear Group,
( u; L& G# C6 T/ a: m' |2 {: c9 ], L7 Z& ?: O/ {% j
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: A9 k. q) A+ H# {' mtherapies. Here is a report from Australia on 3 patients who went off Sprycel5 i( P* N0 v" C; }" N# c
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients" |! l& |8 S/ B1 q" u' ]5 A
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 n2 G$ }7 `8 V% c! e$ `does spike up the immune system so I hope more reports come out on this issue.. O* V5 _5 }7 J! P8 Y
; p% D4 @ Q" U( bThe remarkable news about Sprycel cessation is that all 3 patients had failed3 H" d, Y2 I9 _2 `7 F
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
, x! `# J+ @) z- d' J, Ldifferent from the stopping Gleevec trial in France which only targets patients
: Z$ V& [" U$ v! j% Fwho 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
0 @$ I9 ^! u; N/ o" `9 V! w# wresponse off Sprycel is sustained." C% p" B6 r1 H% A5 B- j6 X0 g# V; C
X- }$ S" _% Y9 k* ^Best Wishes,% X6 W. G& S! {3 Y2 b4 [* a1 l
Anjana* C/ l9 P+ Z/ N
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+ q% B( J- I; ^ k9 H( N+ l% }" UHaematologica. 2011 Aug 9. [Epub ahead of print]$ Q9 C c' d8 a6 R% v
Durable complete molecular remission of chronic myeloid leukemia following
! [- T6 K; N; F( v) U1 s$ u$ N! jdasatinib cessation, despite adverse disease features.5 G0 b o' z& k, o. w
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.4 h8 G$ y7 |, }1 ]3 w
Source
* w( T: r. Q* B9 \, @8 qAdelaide, Australia;! \3 `; M A1 y! n c1 q9 B* y
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Abstract
& Q% f; h2 n9 L+ n& A# \( F: wPatients with chronic myeloid leukemia, treated with imatinib, who have a2 t! Q& j& ]0 L: ?, O
durable complete molecular response might remain in CMR after stopping
6 U1 F, t: U6 i' G; Otreatment. Previous reports of patients stopping treatment in complete molecular
% a6 I3 R' h1 ]2 F+ \/ F( u- Aresponse have included only patients with a good response to imatinib. We* X7 l4 H% o" a: C
describe three patients with stable complete molecular response on dasatinib c5 z. w4 n. h* p) I5 S% N! B# i
treatment following imatinib failure. Two of the three patients remain in
$ | s$ p" b+ _( o; c4 A: Dcomplete molecular response more than 12 months after stopping dasatinib. In
6 Q0 B5 W3 Z& W5 R& Z6 V) [+ mthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to7 T" `& P: N# q( I9 x
show that the leukemic clone remains detectable, as we have previously shown in
/ Y2 R$ n! L1 A5 _3 C* I- Cimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ _9 R3 j: M* s" z' U7 Othe emergence of clonal T cell populations, were observed both in one patient5 e! j% y' r9 O9 \4 ~. a8 N
who relapsed and in one patient in remission. Our results suggest that the- t6 ^7 P# c3 E+ m& v/ X
characteristics of complete molecular response on dasatinib treatment may be
$ i, {- s. n( R3 esimilar to that achieved with imatinib, at least in patients with adverse
! k6 j F+ b0 J3 n. E0 Jdisease features.9 O% m. i6 @+ q
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