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。, T# P' @3 F# P _- h6 D7 q/ W; h
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。: `" W/ ^" R/ |- _8 C
. ?+ F$ T4 m3 }3 a; O作者:来自澳大利亚
6 ]' v" j$ \- V/ ^7 H来源:Haematologica. 2011.8.9.5 ^7 ]3 S+ \: y; N
Dear Group,
2 ~( t8 n& `5 L9 Q! I0 R; T) d: ?3 a( S
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 I; s5 l& ^; stherapies. Here is a report from Australia on 3 patients who went off Sprycel
6 g3 F% R% v1 k5 x- K# d# c/ yafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, u. O) @7 Y# D, r+ z# g3 l; [remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel6 t9 S5 }/ D2 e; A
does spike up the immune system so I hope more reports come out on this issue.
5 @5 H, N7 h; }
3 Y- l# ~ P& e3 R5 Z9 aThe remarkable news about Sprycel cessation is that all 3 patients had failed) B/ i4 T- N- v* }! o# X
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
5 J" G$ C$ E' W/ y9 m% ndifferent from the stopping Gleevec trial in France which only targets patients3 ~$ _5 @5 y" S% c
who have done well on Gleevec.4 p2 b p! P# i$ a* g9 }
6 i- b; `8 H- e& w% N4 B
Hopefully, the doctors will report on a larger study and long-term to see if the
# E( e* C' `9 p9 z2 a3 l. _response off Sprycel is sustained.
. q8 X4 X; g: T: _% U5 j- i) k! f, J: f7 F, h% y
Best Wishes,
6 N- a" [1 f& v3 AAnjana/ W8 G* p9 @7 W/ x
. Q4 I, p% M/ L, c: |, W/ P
2 i/ c9 u/ l: Q( q( {9 y F: T! j4 }5 V
Haematologica. 2011 Aug 9. [Epub ahead of print]% P. s- _; q7 f: P: ]; B1 g
Durable complete molecular remission of chronic myeloid leukemia following
5 s# m% q% B) P9 v. z& D- ?; X/ Ddasatinib cessation, despite adverse disease features.
) M% r- {4 A1 SRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 ]4 O" [) p( M9 B" J; n% q
Source
& k# o/ M1 F4 |$ d0 A0 J! SAdelaide, Australia;( z. p. C9 E% Z8 u
0 [0 k: t4 W6 D" c. x4 SAbstract
9 |1 C6 v0 X5 D3 V: @7 u- x7 c" MPatients with chronic myeloid leukemia, treated with imatinib, who have a. V1 N& u) v) J! @8 T- y
durable complete molecular response might remain in CMR after stopping
- F/ } G' j3 ~, G& A$ [' n8 |treatment. Previous reports of patients stopping treatment in complete molecular
6 h4 u# s5 F/ |4 l7 Eresponse have included only patients with a good response to imatinib. We- Y3 v" _ z5 D& i0 `" t
describe three patients with stable complete molecular response on dasatinib
. q" X; U# G4 b, v0 Gtreatment following imatinib failure. Two of the three patients remain in
# K* s) n6 ]# K9 e) m: V) ncomplete molecular response more than 12 months after stopping dasatinib. In" O+ L4 p9 Q2 _- E7 ^* M
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to5 g- a7 `% U. e! l' T4 d
show that the leukemic clone remains detectable, as we have previously shown in
5 d# L! S. W# ]! x& ~; Rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as" Z5 F" `+ |3 k3 {% g* F
the emergence of clonal T cell populations, were observed both in one patient8 ^2 S4 d' n; Y0 z. M$ m( P
who relapsed and in one patient in remission. Our results suggest that the
3 J/ b6 E; W7 O; p2 |' h0 Echaracteristics of complete molecular response on dasatinib treatment may be
+ d2 p7 ~: B t3 S9 isimilar to that achieved with imatinib, at least in patients with adverse
9 F% L, F4 h. v/ w* q' edisease features.2 @3 J! p* [+ z7 t# }+ d( r
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