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。1 S$ U7 O6 X/ Z$ m. W7 U; h, e/ [" G
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。
; o3 t5 a8 f' S; x8 w
6 }1 {4 J- E1 _# K7 f$ G" J V作者:来自澳大利亚) ?8 [/ \! ~9 }+ L" [5 N# \4 l
来源:Haematologica. 2011.8.9.
% f. ]6 x/ _$ U* hDear Group,
5 L$ @9 @( e2 Q! ` i# F
2 H9 B- ~/ ?5 n1 A5 Y0 w& CSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
' O0 r1 Z1 {8 l2 O' xtherapies. Here is a report from Australia on 3 patients who went off Sprycel1 n% z# A0 K0 G' \
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients# D. \1 e) ~5 Z. v+ _* e- I
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. z' c/ g% h8 H' K7 J8 L5 G
does spike up the immune system so I hope more reports come out on this issue.4 b" B7 H3 J( _2 b3 m# M5 m
* @; I* B: \5 ~$ ]* m, b' ]The remarkable news about Sprycel cessation is that all 3 patients had failed
; r6 U4 ~% ?1 d* i1 Q; G9 I4 A; Q7 bGleevec and Sprycel was their second TKI so they had resistant disease. This is( H' v& v9 v& O% c
different from the stopping Gleevec trial in France which only targets patients- ]) \* E8 V7 q5 I0 w! a# x
who have done well on Gleevec.
5 \9 P& t' J% J% g2 k _- _8 y& |/ Y- _6 \# \$ t4 H1 j7 ^. ~
Hopefully, the doctors will report on a larger study and long-term to see if the1 z) a8 K6 e0 w4 F7 c( h+ \& ?& B
response off Sprycel is sustained.4 i, P4 u9 Z8 c1 y- h! C n! r
z$ u& C9 v3 V7 Y
Best Wishes,& L, e9 S" k2 U0 m# m
Anjana. v+ q; h: g: a: j- @" ]2 C0 J
# Y4 p& g' w ]( N# r6 ^% C9 S2 k+ M m/ t- e! H h
1 t: S4 L) I9 p% n; u5 [! }Haematologica. 2011 Aug 9. [Epub ahead of print]
% ~4 W1 c* x- b$ ?7 mDurable complete molecular remission of chronic myeloid leukemia following
1 |$ A8 N& J0 [$ w1 [dasatinib cessation, despite adverse disease features.5 D* g" M, f4 i% F% w3 L3 R S* s
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
$ {! E& F! D' M, k; m7 MSource; B a/ W: ]" j
Adelaide, Australia;
4 E% E% l* S, {* F4 O* Q1 X# c7 u+ S, p2 O, f/ U
Abstract
. e4 f9 s3 `- J* NPatients with chronic myeloid leukemia, treated with imatinib, who have a1 p; u6 Y5 W7 g# R/ P' L4 J3 O
durable complete molecular response might remain in CMR after stopping/ l. @/ P6 f/ V' M; S* ~
treatment. Previous reports of patients stopping treatment in complete molecular
4 M/ X4 F( C; V. c. J1 X; }response have included only patients with a good response to imatinib. We
7 U6 Z+ R% r: S5 I, Ddescribe three patients with stable complete molecular response on dasatinib [) u7 M& |& B+ }3 J
treatment following imatinib failure. Two of the three patients remain in
4 q7 C- Q2 T: [% Dcomplete molecular response more than 12 months after stopping dasatinib. In( ^" U# j, E; `1 ]; s- n
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to: V1 a9 z% C @* B% Q6 {( r
show that the leukemic clone remains detectable, as we have previously shown in
* A) K9 ?9 o& M. f2 `' {2 ]3 [imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
}# S% }7 ^" O# Wthe emergence of clonal T cell populations, were observed both in one patient
5 J9 M4 d, A3 a# D+ m2 W& iwho relapsed and in one patient in remission. Our results suggest that the$ X' f4 g6 ~3 t4 A: v0 L
characteristics of complete molecular response on dasatinib treatment may be- K) }" l4 j% D7 [- ]- S
similar to that achieved with imatinib, at least in patients with adverse( k+ u# c4 a& ^# V7 i
disease features.
6 p' p/ g; i8 R( |9 s+ j8 ~ |