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 o& G+ t7 J/ \+ ]
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。, v) r$ [ k0 ^' F# C
6 w1 u F8 P% I7 Q! {# m2 n( x" o作者:来自澳大利亚
* V# e% e$ p, p# X: I# _1 v来源:Haematologica. 2011.8.9.
; I: P# u7 s% @, bDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML1 e% K1 _6 o0 ^9 X
therapies. Here is a report from Australia on 3 patients who went off Sprycel5 T3 l4 w8 r! A$ y" \/ t) q
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients; H9 C) f" F' C& Z0 T) K
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel4 N& l% X' T9 n1 u0 X4 |
does spike up the immune system so I hope more reports come out on this issue.8 J$ n1 h* C0 r7 m: w
* t" x/ R# R" FThe remarkable news about Sprycel cessation is that all 3 patients had failed
3 K {& {2 R+ H0 _9 A! QGleevec and Sprycel was their second TKI so they had resistant disease. This is& J) ?9 v0 W$ J, O/ ?; M# l
different from the stopping Gleevec trial in France which only targets patients
0 A/ G: g( [8 K8 \( M- E9 C% m1 ]who have done well on Gleevec.# m& y% V0 I. D, {3 d
$ T, M& E- v# u" W8 M9 LHopefully, the doctors will report on a larger study and long-term to see if the
1 P# s8 }' L, }% F) d! d- Fresponse off Sprycel is sustained.% N; G% `3 f y4 G. |
t/ c' _" m4 s" ^, TBest Wishes,3 `' {% T/ s& c8 e
Anjana; M% h a- l0 z, z# R! u7 _
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1 ?% v; q; G2 F2 |+ e* Y
9 _$ _; ?, I$ r' j; y$ UHaematologica. 2011 Aug 9. [Epub ahead of print]
( N& a- |- }1 c, ~% VDurable complete molecular remission of chronic myeloid leukemia following
" L+ T& P8 H3 ^% n8 ldasatinib cessation, despite adverse disease features.( I5 y$ F7 r7 M
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
5 r: Q& ?8 }2 d" YSource( I) E. |- M* y8 d- G8 s6 P# j
Adelaide, Australia;* u3 ~) R0 j9 G6 h2 v* Z
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Abstract8 J9 T9 y! c7 F+ z
Patients with chronic myeloid leukemia, treated with imatinib, who have a
; A4 {* F' g, I" O3 sdurable complete molecular response might remain in CMR after stopping1 X# f" m7 A1 _& G& M1 p
treatment. Previous reports of patients stopping treatment in complete molecular; ^0 i6 a7 I* m+ h
response have included only patients with a good response to imatinib. We
" }5 n1 ]' U/ ~8 y$ ?describe three patients with stable complete molecular response on dasatinib1 I9 c& p* W Q& S6 _. B2 J( i; N7 {
treatment following imatinib failure. Two of the three patients remain in3 c! R( o4 z7 e/ D& d' u. h9 U
complete molecular response more than 12 months after stopping dasatinib. In0 T2 C& G( v# X% u% x
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
. ]( h( L7 K* k- y' M3 n. J) g- Gshow that the leukemic clone remains detectable, as we have previously shown in. p8 l* B" I& z& Q( H# u' i& g8 p
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as R( {& H0 E8 C
the emergence of clonal T cell populations, were observed both in one patient7 {# D1 G3 X; Q2 `4 Q) D! \
who relapsed and in one patient in remission. Our results suggest that the
3 W1 V+ j+ e, r' O# n) n9 bcharacteristics of complete molecular response on dasatinib treatment may be" |4 @( t% i4 H% ~* m1 ^
similar to that achieved with imatinib, at least in patients with adverse
0 \# h) D2 A( n2 ~# A$ ~disease features.
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