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。8 a6 I) \0 [6 b0 ?" `0 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。
# Y0 }0 \; m! x7 P2 y
% }, n+ P) C, r! K8 R& }作者:来自澳大利亚# `+ [8 k* W2 e2 U* |: V
来源:Haematologica. 2011.8.9.
: ^: R, N% E/ W0 s6 j2 h8 ]2 P3 oDear Group,
1 {! T& F7 a6 y: }! M' S9 A' p2 B2 r7 |& C$ Y2 g7 [
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML* U: q- P& }3 a0 B0 P6 O
therapies. Here is a report from Australia on 3 patients who went off Sprycel
3 Y) ]3 r2 X2 z% K1 d2 a. Wafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients: V+ _4 A+ o6 u. \% X) |
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& U f% j5 C5 I$ M. Adoes spike up the immune system so I hope more reports come out on this issue. q4 G% ?) S; D; S3 l, S
% T# r# ^7 j7 O* y& yThe remarkable news about Sprycel cessation is that all 3 patients had failed7 m, k: c; {. D5 \
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
) e2 x' v1 Y& Odifferent from the stopping Gleevec trial in France which only targets patients
# q5 o4 h( i+ p2 U: y/ s) Kwho have done well on Gleevec.# [. t" c& S8 Q9 B# j
# [4 D9 D6 t9 k* {' ^. THopefully, the doctors will report on a larger study and long-term to see if the- ^& v9 W7 f/ {3 C0 t/ I; _
response off Sprycel is sustained.4 i3 m# X; v! F- e" @+ F
1 V5 e+ O& v: I+ `: e% N- a
Best Wishes,
- K8 B8 [9 u7 |Anjana1 e4 ^' Y& P6 O, ?3 P- f
6 w5 b% K. I8 }; F& y
: j4 D9 o- P/ p3 _- l) B' y3 ^; }% f8 e$ `
Haematologica. 2011 Aug 9. [Epub ahead of print]+ {5 l j3 [; U& C3 B0 K
Durable complete molecular remission of chronic myeloid leukemia following/ X# _: m0 M. Y+ h
dasatinib cessation, despite adverse disease features.
! Q0 j; ~' \+ lRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.- W% m \ z5 J9 A
Source) `3 B+ A* G9 t2 i- |( f3 Q
Adelaide, Australia;
/ ^8 l; `' c4 F! x) g( s( ]8 L# v9 ?- K3 \, ]
Abstract+ I$ q' J( H3 a$ A
Patients with chronic myeloid leukemia, treated with imatinib, who have a2 w1 v& x% {3 Z8 t6 [
durable complete molecular response might remain in CMR after stopping
/ `8 d0 U# @( ~9 Y5 ktreatment. Previous reports of patients stopping treatment in complete molecular
% k& x9 e; t, Z8 k6 Z/ k+ X" hresponse have included only patients with a good response to imatinib. We
: L) r2 g5 K- m% R! }describe three patients with stable complete molecular response on dasatinib
" y' H. w$ i1 }( |treatment following imatinib failure. Two of the three patients remain in9 w Z; k' M2 [" q! `8 s
complete molecular response more than 12 months after stopping dasatinib. In
$ l9 @" A0 R/ S; v% qthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to) k" H- m# l2 u/ O
show that the leukemic clone remains detectable, as we have previously shown in
. r& i" C# U2 x [- kimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 \5 [! |8 s+ x/ s4 T L7 {the emergence of clonal T cell populations, were observed both in one patient( p& K& j* ^4 M7 R- S4 x- q; h/ q/ i, b
who relapsed and in one patient in remission. Our results suggest that the
! H6 |, o: `$ V! K$ P& Acharacteristics of complete molecular response on dasatinib treatment may be
4 v+ I/ |6 e# d/ n- H" ?similar to that achieved with imatinib, at least in patients with adverse
8 Y& Z0 ^. w; m! k4 ?+ E1 ]disease features.
. U4 Q! h7 m+ S e" C" t6 e. M* ]% j |