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。3 z$ H% T; k) x2 E& I5 J
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。
3 D+ U& w& \' ]9 h6 o4 M % q( b" F0 w+ [8 \: g- d
作者:来自澳大利亚/ i" B- F/ P! U: Y7 S% a' h+ J" z9 g
来源:Haematologica. 2011.8.9.
2 u- R# Y) d9 c; PDear Group,
& H5 r( n+ p5 m
4 }; A+ X7 I8 }9 |Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML% ?9 k; G" u# p3 U# A+ l4 \& X5 A5 P
therapies. Here is a report from Australia on 3 patients who went off Sprycel3 O* B5 ]: V" G. I0 G3 @
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients8 V/ M7 u& i- z* k* X7 m& _: q' l9 @
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel' v/ @9 k- D, ~' F
does spike up the immune system so I hope more reports come out on this issue.
% c9 @2 f: o. T6 v* m
, V5 Z8 q2 o5 \+ B# e2 MThe remarkable news about Sprycel cessation is that all 3 patients had failed- j8 g+ b5 V5 i- n: Q
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
" y0 J1 V. }7 Q A6 cdifferent from the stopping Gleevec trial in France which only targets patients
5 k& P0 V" _6 t! Pwho have done well on Gleevec.
( p( ~& y. J$ a+ S; \) y0 |1 X+ V/ \6 K, V
Hopefully, the doctors will report on a larger study and long-term to see if the
8 n5 J5 {" k5 u' M" C" C# presponse off Sprycel is sustained.7 V @8 u8 A; Z, e# ]
2 `! m. X* M, Z8 U
Best Wishes,
, p1 T' q+ G9 eAnjana
9 i! W: ]! e( P9 M7 K5 Z. s, n
" E4 c3 ?* Y" M# ?/ z6 z8 m: ~* B6 h. \4 n7 E$ ^
) O! I ^$ a9 g. V: w5 AHaematologica. 2011 Aug 9. [Epub ahead of print]
/ ^+ x" Y6 G% h& |. K' G5 t% ]Durable complete molecular remission of chronic myeloid leukemia following7 m/ p6 r9 H) e
dasatinib cessation, despite adverse disease features.) M9 W3 G8 U' n$ p1 q) t
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP., b4 E2 D- r, p
Source
6 W' t8 D( L/ ?( c V, }" pAdelaide, Australia;
; O& R9 u" {) L% Z e, K m' ?$ K* v1 q
Abstract
; k1 ?; Z: B9 ~* L6 F5 D( h. M! IPatients with chronic myeloid leukemia, treated with imatinib, who have a) d; ~" X" U1 T6 f
durable complete molecular response might remain in CMR after stopping% R7 M* c2 V" j; P. m5 e- M7 X
treatment. Previous reports of patients stopping treatment in complete molecular
, r$ X7 n' }1 b6 T" |response have included only patients with a good response to imatinib. We
/ }1 W; R/ ^! y: U: Z/ @describe three patients with stable complete molecular response on dasatinib6 W) h- V$ @3 T$ L
treatment following imatinib failure. Two of the three patients remain in A- |& m2 ^2 f9 \% F; x9 m. n
complete molecular response more than 12 months after stopping dasatinib. In
% X5 l' r; U* @1 C: p. N/ d9 rthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
0 z, A# S: V( x5 j/ S5 |, rshow that the leukemic clone remains detectable, as we have previously shown in& `2 c' h/ u' M3 p
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as/ b2 X5 _1 _8 s1 C
the emergence of clonal T cell populations, were observed both in one patient; J) H* ~# [* ?' ]. \( p6 [
who relapsed and in one patient in remission. Our results suggest that the" U* ^( k9 s8 ^& J2 |$ A0 f
characteristics of complete molecular response on dasatinib treatment may be8 m4 r6 O: l$ k. S, p" s
similar to that achieved with imatinib, at least in patients with adverse
' z4 X* ]" @2 r" X1 pdisease features.4 w" }8 }: g( ^. E; P3 o
|