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。5 q8 g- _" i' r% P7 U
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。+ \( H2 E+ A u, \
7 Q- ^; S, _1 l+ c1 @ g作者:来自澳大利亚; i" U; ^* ]: f3 j
来源:Haematologica. 2011.8.9.+ i. `* V( r$ w
Dear Group,5 { z) B, f0 O" t5 h* S, c
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" D/ @/ a" i3 N, d* E$ X
therapies. Here is a report from Australia on 3 patients who went off Sprycel! i+ h; w F' A
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
1 ^2 J: M$ s7 r; f! Kremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 F( h8 q9 ]4 a0 L9 X$ S
does spike up the immune system so I hope more reports come out on this issue.8 l$ C/ T1 R! d& T7 g
2 x, W! y3 T3 Y& X) [0 EThe remarkable news about Sprycel cessation is that all 3 patients had failed
* f5 ?8 i4 O5 p7 K% i0 W0 u: j1 sGleevec and Sprycel was their second TKI so they had resistant disease. This is
' {* o4 H* X% w; f: x* M2 Gdifferent from the stopping Gleevec trial in France which only targets patients
& ?) q: B6 C9 y9 w. mwho have done well on Gleevec.
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% e6 x# x5 H& l% x$ B* ?Hopefully, the doctors will report on a larger study and long-term to see if the
& V. a. x7 h. V( Iresponse off Sprycel is sustained.
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% f& ]8 |) J( p: KBest Wishes,
- q& T- K5 b- ?- S; FAnjana" t! Q; W' y1 t3 c, e
( v% j. e- m! y& H7 f; t- C
9 e( j( m& q. o. I/ S4 g, O
9 s, @0 t, Z9 N WHaematologica. 2011 Aug 9. [Epub ahead of print]* ~3 ?- y( [- ]. U
Durable complete molecular remission of chronic myeloid leukemia following
0 g/ _7 P v6 kdasatinib cessation, despite adverse disease features.
1 s8 e: X4 X% ^3 S, n z. H) p' \Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.5 s! }' L, Z1 M6 o% W# ]: @
Source
8 F( S9 T( Y; \2 ?, uAdelaide, Australia;2 ]- Y# `& a0 f, T( j& h8 Z' F4 ]
# z: ?0 I: R: {5 Z! ?( CAbstract' |) E9 z/ n3 \2 D% ~8 A3 e
Patients with chronic myeloid leukemia, treated with imatinib, who have a( Z& b0 O# y" c2 h: v; S
durable complete molecular response might remain in CMR after stopping0 s9 M6 i; {$ ]. `
treatment. Previous reports of patients stopping treatment in complete molecular5 P( a' w( i G: j7 |( e4 ~
response have included only patients with a good response to imatinib. We
3 j4 A% @9 l# t5 X# y" Y/ m4 C8 Xdescribe three patients with stable complete molecular response on dasatinib# F1 q3 S. }) f; L! n
treatment following imatinib failure. Two of the three patients remain in/ }# U: }9 D, ~
complete molecular response more than 12 months after stopping dasatinib. In+ b, c/ ]5 H2 @- \3 R4 _2 \% a
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
0 h \5 P A: l' k& n: M) i" V, \show that the leukemic clone remains detectable, as we have previously shown in
% F, j* f9 v, C# ?/ K) Nimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
% L3 K6 c! s8 L9 |% n& ?# d$ F1 j7 vthe emergence of clonal T cell populations, were observed both in one patient
4 R2 {$ ~3 X; z7 s; O9 o5 L0 Jwho relapsed and in one patient in remission. Our results suggest that the2 ?2 g/ V2 \$ }- O8 u
characteristics of complete molecular response on dasatinib treatment may be
1 l; o L }' V5 ]$ D( ysimilar to that achieved with imatinib, at least in patients with adverse
3 X; I+ S( D4 K& G2 Vdisease features.
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