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 O6 X# j0 G/ N' |/ E1 Y* @ 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。
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# o! S) K2 E1 O) p+ l" o作者：来自澳大利亚( i4 b. t- l* o. v5 {$ {" e
来源：Haematologica. 2011.8.9., ]. L4 \8 o2 k( n1 z# b
Dear Group,' Q; C/ Q# r# {0 b, I; \$ _
$ J/ x* U1 N T0 xSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
5 D' }6 h% Y- C4 y$ T7 T6 e) rtherapies. Here is a report from Australia on 3 patients who went off Sprycel0 t+ d. |/ R! m! W
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
6 e5 ?/ {% _5 G7 l, {remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel5 Z- G, b7 a! |) J+ H8 C7 E& p9 |
does spike up the immune system so I hope more reports come out on this issue.; X" U$ I/ ?- S: U) c% B1 _
: [. i; g' R" h6 S
The remarkable news about Sprycel cessation is that all 3 patients had failed
2 X- q* x; e7 G+ o6 q$ FGleevec and Sprycel was their second TKI so they had resistant disease. This is6 v1 z5 t8 N* F1 z$ d
different from the stopping Gleevec trial in France which only targets patients
+ I$ A! `9 t2 c. c6 |$ Xwho have done well on Gleevec.
/ R; K" J k$ y( Z* g9 M1 w
7 D; }$ K. B! J7 I& z. {Hopefully, the doctors will report on a larger study and long-term to see if the5 A3 C R! | u9 d- V
response off Sprycel is sustained./ Q* N" R; B5 `0 L- b' B
% i4 [4 o i. n0 s) f" QBest Wishes, n% S3 K* ~$ N( H7 j7 s
Anjana q4 E; ?( _7 d7 J) N( f
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, x: t5 E/ h4 _/ J8 I3 _) \
. ? X- \$ R i9 L% ?* o4 t' y1 SHaematologica. 2011 Aug 9. [Epub ahead of print]
2 Y: n7 K9 y' n0 q- H6 X& w" j6 fDurable complete molecular remission of chronic myeloid leukemia following
' ~6 ~* \# C( ]& {1 \, Mdasatinib cessation, despite adverse disease features., B" ~% M9 A- x6 c5 |2 P
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' [ W# P: c- K3 @6 _
Source
0 s# `3 L% O, \& B2 x! D- }* VAdelaide, Australia;
; H3 W4 [1 K$ N, F* N& b( B3 U4 K# d9 i9 z4 t
Abstract3 Q: w, E, X3 ]
Patients with chronic myeloid leukemia, treated with imatinib, who have a! `- P$ @: d" }6 K# \
durable complete molecular response might remain in CMR after stopping7 z/ c: k" S( j4 c2 u$ h
treatment. Previous reports of patients stopping treatment in complete molecular
5 L& g: P" T! y% y+ e4 H$ Eresponse have included only patients with a good response to imatinib. We# a) ~0 ~: {% J, R
describe three patients with stable complete molecular response on dasatinib
# f- G' o& D/ {7 A: r9 I/ ~treatment following imatinib failure. Two of the three patients remain in; ^4 l, h, }' S+ w. K3 h! c
complete molecular response more than 12 months after stopping dasatinib. In
, j% j. ?5 P0 u- cthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to/ B, Q% F& l: [. {1 z4 B
show that the leukemic clone remains detectable, as we have previously shown in5 A0 y/ j$ c" b3 _
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
}9 a" A8 M0 ]! z) Athe emergence of clonal T cell populations, were observed both in one patient
. X! Z$ [6 X3 S$ f, }1 Awho relapsed and in one patient in remission. Our results suggest that the
. X3 V5 A6 }# p) a; Ccharacteristics of complete molecular response on dasatinib treatment may be
8 ]% a y+ M$ |0 q. _3 w- Osimilar to that achieved with imatinib, at least in patients with adverse2 {7 Z9 Y; v( p2 f. k$ L0 q
disease features.- N- g& K; ]4 ^1 k( \
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