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 y. T" n. z, h9 ` 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。" _/ T" P7 E( m) X
# a$ J; u: u! h& k7 z作者:来自澳大利亚
7 P# t, \8 A, j% g) k2 j' M9 q来源:Haematologica. 2011.8.9.
% b/ b) D; n$ o) h0 o" T0 p) sDear Group,2 w6 n0 Y( ^- R; b& ?! C5 d7 i
! `. j4 d8 W; O7 mSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, J( d% ?' Z2 Y: ytherapies. Here is a report from Australia on 3 patients who went off Sprycel! e8 f& g/ P% G4 s
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients6 J( W+ w8 Z1 v/ U/ z5 B
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
. |% c( E' f. H( l3 |does spike up the immune system so I hope more reports come out on this issue.# t9 m( b0 v/ h! b+ `, s Y7 y: G
0 V% `$ R. {$ v! J6 u* p; [! UThe remarkable news about Sprycel cessation is that all 3 patients had failed
1 f( J& n% k) G$ ^& CGleevec and Sprycel was their second TKI so they had resistant disease. This is& K6 g9 L. _5 `' R T" {
different from the stopping Gleevec trial in France which only targets patients- s* n0 R: _* Y8 V" h4 \. X
who have done well on Gleevec.0 k) {0 J% S. ~
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Hopefully, the doctors will report on a larger study and long-term to see if the
" A9 L8 B9 w& S* s8 T. q' D2 D0 Sresponse off Sprycel is sustained./ f) d4 R: A$ f; Y. `4 u* R
9 F6 f7 n$ T$ Y
Best Wishes,% E: a' J3 D8 t. z
Anjana
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3 h) z( w) P1 ]: KHaematologica. 2011 Aug 9. [Epub ahead of print]) x, r+ B% {' f) {
Durable complete molecular remission of chronic myeloid leukemia following
+ r, D$ {$ w7 U+ l- W. zdasatinib cessation, despite adverse disease features.$ e" B4 {9 G9 M3 j$ ]1 \8 x: g9 Y
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
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Adelaide, Australia;
3 ?% X5 u/ @( }
3 G3 w5 ~# D- l R5 {( F0 c, ~) zAbstract
$ q4 U ~: Y* W/ R% HPatients with chronic myeloid leukemia, treated with imatinib, who have a& ^7 y/ u; o# ?4 }# }) b" T
durable complete molecular response might remain in CMR after stopping0 t& g+ p9 z1 ^' l7 [; h) `( l" P
treatment. Previous reports of patients stopping treatment in complete molecular* n+ {, Z" Q3 M5 H8 B C
response have included only patients with a good response to imatinib. We
4 |* q! k% {: }, S6 w) Y7 V% ldescribe three patients with stable complete molecular response on dasatinib! G' `( g& F# J2 j5 i0 d' x
treatment following imatinib failure. Two of the three patients remain in( ^$ M+ j6 {5 g3 p
complete molecular response more than 12 months after stopping dasatinib. In" C4 {" ~+ V/ L P, f f* ?" B
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
# v* q# w3 a! E7 u; m- M. A) s8 ]show that the leukemic clone remains detectable, as we have previously shown in: x3 L$ R" u, v/ `( u! V; t
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
7 F. @. d2 ^* Z8 z/ ~the emergence of clonal T cell populations, were observed both in one patient1 U& F3 z" E* ~, i+ R( q. w
who relapsed and in one patient in remission. Our results suggest that the3 r1 n V t3 {+ }
characteristics of complete molecular response on dasatinib treatment may be
4 E8 }0 `1 x, R. z- nsimilar to that achieved with imatinib, at least in patients with adverse
* c1 ^: G' p3 i- [, ydisease features.
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