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。 l. R$ O3 B5 u j8 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。
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作者:来自澳大利亚+ T' Q6 M |$ Q) d }0 s, Q* Z' B1 L
来源:Haematologica. 2011.8.9.% O1 w4 f' P( C+ w: Q
Dear Group,! G B. f+ u. H2 S. D+ Q2 S* i
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 j% F0 ]& l& G I/ H- \& ]; T7 ]+ xtherapies. Here is a report from Australia on 3 patients who went off Sprycel
" E$ D" C/ a1 U( n: \- q Safter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
8 t6 h6 V- V! `+ J$ i& R- N1 tremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel7 T6 b% k& @6 A% R
does spike up the immune system so I hope more reports come out on this issue.2 [: q! F. O6 e& n/ P
6 u1 |' y3 S0 s/ D9 WThe remarkable news about Sprycel cessation is that all 3 patients had failed
5 f& E6 t; ]/ f) QGleevec and Sprycel was their second TKI so they had resistant disease. This is
1 q; X' `# {' ^/ m$ D9 U% mdifferent from the stopping Gleevec trial in France which only targets patients
7 j/ ~% F7 n$ c0 l! v8 o( iwho have done well on Gleevec.8 T# S3 G2 `8 {# X8 B
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Hopefully, the doctors will report on a larger study and long-term to see if the
8 C9 t* V* h; Q: W' bresponse off Sprycel is sustained.
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Best Wishes,* [9 Z @; J. D( j
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
4 [2 p& L- ?" L2 M& {5 T2 UDurable complete molecular remission of chronic myeloid leukemia following
5 Y$ g. \) T( i4 S% `# `+ sdasatinib cessation, despite adverse disease features.1 E6 C. x" ~4 ^( ]# i
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.- }3 M2 @1 N$ e, @8 A
Source" u+ |' s2 l: U8 \/ ?* H: B; ^
Adelaide, Australia;% Q; P' U, W! C$ T$ E i
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Abstract( b9 V' l, R- a
Patients with chronic myeloid leukemia, treated with imatinib, who have a
1 s& N2 W [* w4 J# `3 J9 w5 zdurable complete molecular response might remain in CMR after stopping
. y/ m9 e+ c! L; x0 Q ~/ t4 p9 @, ptreatment. Previous reports of patients stopping treatment in complete molecular
: a/ F8 S1 u$ ^: c# u" {response have included only patients with a good response to imatinib. We
* ?! s4 ~5 U, w) y6 R( j+ Bdescribe three patients with stable complete molecular response on dasatinib% u* D+ u% i X) _0 c2 W$ @" Z9 M
treatment following imatinib failure. Two of the three patients remain in
. o" s9 U# C( x: M" q ?$ f8 T. wcomplete molecular response more than 12 months after stopping dasatinib. In
& } l2 E+ h# U$ ithese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
9 U! N) D+ A$ }: K. s5 gshow that the leukemic clone remains detectable, as we have previously shown in1 D+ ~+ y. Y% A
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as( M& _9 B! h6 D. D3 F7 \
the emergence of clonal T cell populations, were observed both in one patient& C4 U8 o- K' K; m2 Z& v6 \0 ^" j
who relapsed and in one patient in remission. Our results suggest that the
7 R* P- |; F% `/ ncharacteristics of complete molecular response on dasatinib treatment may be
3 a# x8 P. y( gsimilar to that achieved with imatinib, at least in patients with adverse
9 s$ H @3 H( {$ Xdisease features.
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