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。
2 P' y$ }; K2 M0 [$ X 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! Z; s. b% b4 _' m/ ^
' s& K3 m* l( y7 x7 q
作者：来自澳大利亚
" H6 @5 Y6 r4 q, {/ e来源：Haematologica. 2011.8.9.+ G' V& G# V: ]
Dear Group,
( \1 Z' w/ D3 q
% {) u8 k: t, }! ]3 j! ^. f' rSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
7 m5 [9 N( ?0 {3 G9 s% I! g4 R( [) v; rtherapies. Here is a report from Australia on 3 patients who went off Sprycel4 h* b6 O0 C M) j+ t _2 d8 Q
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients9 J& F; Z: t4 D- H1 ?+ R& r( ]
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
8 `' ~1 L' `: W8 `9 bdoes spike up the immune system so I hope more reports come out on this issue.
3 v, E! q j/ r
( _7 P! m* J! h) i5 qThe remarkable news about Sprycel cessation is that all 3 patients had failed$ j, v* N) l! T5 q; ]) \6 N. c
Gleevec and Sprycel was their second TKI so they had resistant disease. This is. K( N0 k5 x1 m8 ^" L, s$ \/ a
different from the stopping Gleevec trial in France which only targets patients6 G0 J; y3 e. ]. t2 h) L
who have done well on Gleevec.% T3 s, Y1 |) q1 D7 _
/ N+ O- d: V& F9 B
Hopefully, the doctors will report on a larger study and long-term to see if the
3 z6 r3 p0 [0 ?' h. cresponse off Sprycel is sustained.
8 k5 G9 H& \- i
5 d2 l/ E' u4 m! ^3 W) n3 w2 k' hBest Wishes,# W9 _! Y/ u! G w8 I) B
Anjana. ]- F. b% k2 U- M
7 j$ }7 T$ ?, \4 ]7 O
0 W$ h V% J& u' c; b
5 D9 `( x d9 Z+ SHaematologica. 2011 Aug 9. [Epub ahead of print]; B6 [: `- N7 |% U
Durable complete molecular remission of chronic myeloid leukemia following4 u* j3 {; X a1 `6 Q! ^
dasatinib cessation, despite adverse disease features.
! {! ~$ _, g5 [+ P# fRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP. u: m6 r1 p; `: m5 a, d
Source
' ^9 r7 X# V1 p3 h8 VAdelaide, Australia;, E: K# o- |( ?. M8 t+ O
1 A) y5 h! @5 P7 f( X$ SAbstract1 Y' ~) ~. a1 ? i$ w& B
Patients with chronic myeloid leukemia, treated with imatinib, who have a3 y1 V: t, ~& v! w9 f4 _
durable complete molecular response might remain in CMR after stopping: q5 ]0 F1 f' N% c% L" ~
treatment. Previous reports of patients stopping treatment in complete molecular+ u, h( h& o. A& B; z0 k' Y
response have included only patients with a good response to imatinib. We2 j z- ]+ _7 p
describe three patients with stable complete molecular response on dasatinib* z+ {/ k0 h2 t$ h/ e
treatment following imatinib failure. Two of the three patients remain in
Y" P3 Z8 K8 C* _, e1 fcomplete molecular response more than 12 months after stopping dasatinib. In' o9 o& {5 L, y0 K3 O
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to( b5 W5 J j' U2 j' B$ s( o) u6 @8 M
show that the leukemic clone remains detectable, as we have previously shown in
' z6 \1 e9 w, F- jimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
9 Z' c6 A5 k7 I' I5 ithe emergence of clonal T cell populations, were observed both in one patient
, n7 c5 x# R; E* {+ twho relapsed and in one patient in remission. Our results suggest that the. e' M$ ?+ Y2 e. J# d
characteristics of complete molecular response on dasatinib treatment may be+ i# ~* S; b% _
similar to that achieved with imatinib, at least in patients with adverse
8 Y4 \8 c: j9 i# sdisease features.
! k0 f# M- _7 U& e2 ^5 A) c: U) V |
显身卡
