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。
( q N0 l" @7 s# N+ x$ X: z 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。4 ^. W1 ~, L+ b' ^, g8 b$ v4 N
- {6 {/ N8 d u作者:来自澳大利亚
/ @) r3 U$ ?/ O0 r! Q来源:Haematologica. 2011.8.9.
: u# b. S a" A; ^9 W- f* W, C+ y. cDear Group,. }; Y( D6 L5 [; c+ S. p2 `' T
0 M- s0 B/ L- h) W$ SSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
8 Y1 c( ]5 M/ b# A1 Htherapies. Here is a report from Australia on 3 patients who went off Sprycel) } K2 m9 {3 X" h, V E
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ [2 R% B: f; @* f7 b& hremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
* z) J2 t% p1 n5 G% Rdoes spike up the immune system so I hope more reports come out on this issue.0 e% r; p" ]/ x' @; {$ ~% I r
; ?6 H; D' S9 I4 `8 \4 w: l; B3 cThe remarkable news about Sprycel cessation is that all 3 patients had failed
% g! P/ ? ~9 FGleevec and Sprycel was their second TKI so they had resistant disease. This is$ M8 w# a/ Z9 W3 }* P! P B+ }
different from the stopping Gleevec trial in France which only targets patients
; _+ ], z' ^8 T" Y; ~who have done well on Gleevec.& q3 {8 D- u0 e5 ?+ @5 A( X# M3 g
3 C2 ~' L8 J- hHopefully, the doctors will report on a larger study and long-term to see if the6 a3 r, A7 W6 M) [5 i Z' r8 e( j
response off Sprycel is sustained.
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2 f0 d3 W: r5 i7 [* E0 QBest Wishes,
. ?" `" H# u5 q+ u, aAnjana# X' U- i: t9 }* s9 ^5 V* l/ T; o
: ]* p% a% z- G; y W( b( r/ u. r
5 L0 ?* B( `- r1 v" L8 k8 c- {7 m- n
. e$ \, O" |1 N* v, r8 u4 ~- T' fHaematologica. 2011 Aug 9. [Epub ahead of print]
% G9 C' P" T/ I' V# G! m7 F( r- VDurable complete molecular remission of chronic myeloid leukemia following
, Z) L# J5 k2 Ndasatinib cessation, despite adverse disease features.
9 m, ]" {4 t+ O) Z- a7 zRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.& u9 K( b9 C6 g3 t- q
Source
( y0 W! \* Q; q* X; H& U7 BAdelaide, Australia;. D2 D# Y& x- X* h+ j: U: ~
% [' C1 n8 `: I6 h7 t! h9 J) l
Abstract
$ a4 E( q) R3 O) W/ NPatients with chronic myeloid leukemia, treated with imatinib, who have a- d+ [2 h% m7 o! U
durable complete molecular response might remain in CMR after stopping
- O; s5 ]4 d+ q3 c+ |treatment. Previous reports of patients stopping treatment in complete molecular
; o. Q& U( R/ p, y" ^( \" lresponse have included only patients with a good response to imatinib. We& Z. |/ ?7 P- a% f' i& f
describe three patients with stable complete molecular response on dasatinib
; S4 J# \/ U3 l) T4 w/ Ztreatment following imatinib failure. Two of the three patients remain in
: H+ j) s7 [7 }/ D2 Q+ p. mcomplete molecular response more than 12 months after stopping dasatinib. In0 p r+ J* @' v, ~/ h' S, H! w
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
1 Q* }0 Y# [7 Q5 j' t% ]$ dshow that the leukemic clone remains detectable, as we have previously shown in
+ J( b: H. M' fimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
: P* D* }$ n8 i5 I% K mthe emergence of clonal T cell populations, were observed both in one patient' N- o7 f7 @* G5 ^
who relapsed and in one patient in remission. Our results suggest that the1 R( b! |+ W" I) S6 J
characteristics of complete molecular response on dasatinib treatment may be
% X% N$ k2 Y: r( ?" [( Z$ j" G- @similar to that achieved with imatinib, at least in patients with adverse
/ i" f1 g. S, \& Ndisease features.
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