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。0 @: y% z2 e" t7 f5 a( q. P
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。/ U0 [5 Q5 x6 L: E* ?8 E+ D/ i( ^
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作者:来自澳大利亚 S; M) _/ L5 p4 a0 U, E7 i0 z
来源:Haematologica. 2011.8.9.# F$ H& \! b& j( v' A1 j5 u# X
Dear Group,
5 o0 p1 `4 @1 d- S; A0 M9 ~0 T
8 V* E# J, \9 n$ N; RSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
1 k! j, j8 w# j+ z; Vtherapies. Here is a report from Australia on 3 patients who went off Sprycel+ e. l, t$ {5 ?
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 L* \6 `# |! premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' I5 W* X6 C/ L5 c) k- y5 b ?
does spike up the immune system so I hope more reports come out on this issue.
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& d0 n6 y/ B- uThe remarkable news about Sprycel cessation is that all 3 patients had failed
" ]0 x/ Q- P r B* cGleevec and Sprycel was their second TKI so they had resistant disease. This is
; W- R% H5 \) j) }( ^) A- ?different from the stopping Gleevec trial in France which only targets patients
' m# o9 N; @! e# \- x" G2 ?/ qwho have done well on Gleevec.% {' o7 V8 K& M
6 f1 \4 H. \8 ^2 j4 B7 sHopefully, the doctors will report on a larger study and long-term to see if the
! s7 [2 o x. p7 V$ t0 C+ Cresponse off Sprycel is sustained.6 b m4 o* p; K( C0 z& p0 k! O
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Best Wishes,
3 K# G4 R! l8 f4 U7 N1 ?Anjana
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+ z. ^, ?) Q; L( o8 a; L# @* u) V9 t! n& V5 n' @! c3 i
Haematologica. 2011 Aug 9. [Epub ahead of print]' u4 Z/ ^' A3 A5 c! I
Durable complete molecular remission of chronic myeloid leukemia following
" e; |- e3 z+ ^, Z" ?dasatinib cessation, despite adverse disease features.4 ]2 f2 {1 S; z; T- C2 J4 X
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.0 `/ Y7 K$ K. t# r
Source1 r9 J7 C: }0 {* @$ Y. Q& R
Adelaide, Australia;
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Abstract
) P. ?3 Z; N( p% IPatients with chronic myeloid leukemia, treated with imatinib, who have a
" y2 {$ n! N7 i' h: c( h& bdurable complete molecular response might remain in CMR after stopping
9 C) O% y# p6 k2 L; jtreatment. Previous reports of patients stopping treatment in complete molecular, \+ R1 t. W1 l4 d* E; M6 c+ M
response have included only patients with a good response to imatinib. We- g- [' H J5 L1 G6 S- T6 q
describe three patients with stable complete molecular response on dasatinib5 h5 M7 i+ k2 U7 U* r3 }/ R: [" p
treatment following imatinib failure. Two of the three patients remain in8 _2 r# ` d* n! n+ b3 P
complete molecular response more than 12 months after stopping dasatinib. In- u% E! Q+ s0 W9 z# k
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
6 g5 i- O1 z3 Y# l3 H( Hshow that the leukemic clone remains detectable, as we have previously shown in
' O5 L3 C" Z# T. [' R+ A- S( ?imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
) s' t4 { _/ b5 Bthe emergence of clonal T cell populations, were observed both in one patient4 X) ~3 L: R$ j& Y7 c* F
who relapsed and in one patient in remission. Our results suggest that the' N2 U$ E( a2 P4 r: |; T
characteristics of complete molecular response on dasatinib treatment may be
2 g8 W$ j" w' |) @similar to that achieved with imatinib, at least in patients with adverse
2 C O* N' u/ Jdisease features.5 X/ k5 l& G+ O: X. K# b
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