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。
# Z& }$ r3 P) P9 ]- W 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。- J$ I0 v& @3 f7 J/ g, R1 Y
2 ^# b% w/ {! H( Q [8 I$ C% b0 T作者:来自澳大利亚
, {8 G. Y4 W* P0 {* N8 x来源:Haematologica. 2011.8.9.
; G' K0 n. C' S: l0 Q6 j$ _Dear Group,! }' M0 \! F/ `7 S* { I, ^
. J& Q/ ]; b; X4 ^8 I3 w3 L* i4 @$ g; RSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, D0 s* N4 H% q M) n* q% p: U8 ztherapies. Here is a report from Australia on 3 patients who went off Sprycel* u& O) N: h: x
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
! N- H$ m9 W& ~5 B# V9 a( f; kremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel0 {5 S2 k6 T# N' S: ^
does spike up the immune system so I hope more reports come out on this issue.
' P6 v2 {3 s% @$ f
l( V5 I2 x# L+ N( H8 p0 r& ^The remarkable news about Sprycel cessation is that all 3 patients had failed r4 h1 e% s5 G# G
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
5 H1 N* Q+ J/ T# Mdifferent from the stopping Gleevec trial in France which only targets patients5 z$ {) [+ ?& U* s+ Q$ ?1 E* D
who have done well on Gleevec.
g3 \9 o1 S' V# B
. I' \& a% D, nHopefully, the doctors will report on a larger study and long-term to see if the( I& V5 Z, d3 u. l
response off Sprycel is sustained./ s% }# |; A1 U+ ?! A$ S2 K6 A9 j
, q9 {7 E& |0 B% r# u- DBest Wishes,5 M% K( l7 r' i- f
Anjana1 J) c: H' m7 ` _+ _9 w2 p
. ]8 @! B( V; l3 S' r: I
, D, G/ @& x( n. y3 a9 s6 J. ?
* z6 u2 g' y5 v2 ?0 xHaematologica. 2011 Aug 9. [Epub ahead of print]3 F( Y- z) R- p7 E# U! a/ K
Durable complete molecular remission of chronic myeloid leukemia following
/ w0 o: a7 _6 udasatinib cessation, despite adverse disease features.& c& n9 Y$ U( @5 @2 P; U1 t/ ~
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
( O- \. O$ o/ {: R: N) ISource
% j/ p/ G" n0 a( jAdelaide, Australia; P- V0 ]2 ~2 c0 {# v
+ }& P5 Y& K% k! N/ k3 ^4 |
Abstract
4 H1 }( j. q; ?/ m ?9 A0 y" lPatients with chronic myeloid leukemia, treated with imatinib, who have a
1 k, J/ p+ x+ X. Zdurable complete molecular response might remain in CMR after stopping
$ K( G5 m. X, U% @+ B% Ktreatment. Previous reports of patients stopping treatment in complete molecular8 C% b0 E+ d2 ~- T
response have included only patients with a good response to imatinib. We
; V/ D/ z9 }: z$ ]4 J% y7 y. v& v* B, Odescribe three patients with stable complete molecular response on dasatinib) Q' F2 C; e0 [
treatment following imatinib failure. Two of the three patients remain in
6 [5 ^3 \" u. Hcomplete molecular response more than 12 months after stopping dasatinib. In% K/ _- Y0 G2 p: y
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to! P2 g& a! f- G- P
show that the leukemic clone remains detectable, as we have previously shown in
! g: a- O; R( {- ]- H# K2 I9 vimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
: J% i6 D: L# _the emergence of clonal T cell populations, were observed both in one patient% X# a( `5 i" }, w; R! O& }5 `- Q/ ]
who relapsed and in one patient in remission. Our results suggest that the
" B, G( h2 C7 S; k- {characteristics of complete molecular response on dasatinib treatment may be
+ M" ~; d; `7 ~( ksimilar to that achieved with imatinib, at least in patients with adverse
3 n; R5 y! f9 q6 E9 {4 Mdisease features.) f& C1 g! _1 w$ l
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