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 F4 t! G7 l. M: t6 n8 D. u 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。7 j7 u( ^# S' M* v# C& k, v
6 X; p9 Y' y+ c2 Z作者：来自澳大利亚8 ]3 Y, Q/ l2 `3 o; \ ]2 {
来源：Haematologica. 2011.8.9.( \& @7 ^" X4 ~% S8 F: k# c
Dear Group,6 x) x% o! C1 _
) t3 r! {9 }( w$ ?$ z% R
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML: }/ S1 p% {* w1 p p; c- _
therapies. Here is a report from Australia on 3 patients who went off Sprycel+ c/ u4 ]# \# ]8 b6 {& U
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
; r( k2 t3 ?' s" T% S L/ {& |5 m% k( dremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
$ q) E0 {$ _3 e! `does spike up the immune system so I hope more reports come out on this issue.- w. V( d# X/ S$ \3 ~8 `' g; d
' o4 T! Z. b9 O! g( V% t
The remarkable news about Sprycel cessation is that all 3 patients had failed
% W* m* F$ U4 [7 DGleevec and Sprycel was their second TKI so they had resistant disease. This is
7 D3 X$ V$ Y5 b1 E5 k& N$ ~- e- n! Sdifferent from the stopping Gleevec trial in France which only targets patients
# ]& ~4 V }4 M, F" x" Lwho have done well on Gleevec.! S, f% T( y: g6 C' {
! n( j* ]! t [! W% L( T7 PHopefully, the doctors will report on a larger study and long-term to see if the
+ f1 J: U- p' E0 Y1 dresponse off Sprycel is sustained.
: L1 l! | ~9 J( R* R
( B2 g" b0 ~5 \" `+ fBest Wishes,
5 p% W$ R: @- i6 R4 q7 O0 p4 qAnjana
9 {% {2 }7 C- F) \5 |0 M) v+ Q# h: C; R5 X( f& \1 }$ G; Q6 d
/ t. Z9 {$ m1 j K/ n8 G
* N2 O& I5 j+ Q5 P, @: kHaematologica. 2011 Aug 9. [Epub ahead of print]( y( B$ b/ B$ l2 p% k( @
Durable complete molecular remission of chronic myeloid leukemia following4 ^6 E) V0 Y8 ~% c6 U8 A: F
dasatinib cessation, despite adverse disease features.
# ]& }2 N3 _+ E( e6 ERoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
- X% X6 ~/ a+ K; SSource+ ~/ x% @' \/ B- K, N. Z5 W( \
Adelaide, Australia;0 x2 q9 L' J i, l
; l% ?; O( O3 |: L, S! ^$ n4 o: @$ t/ oAbstract
$ ?$ S( m S; x0 ]6 s- mPatients with chronic myeloid leukemia, treated with imatinib, who have a! A: K- _. Y& R% a2 _' w' e0 P
durable complete molecular response might remain in CMR after stopping/ j$ Q4 G5 d4 x0 N% x6 P8 w/ V: Q2 R
treatment. Previous reports of patients stopping treatment in complete molecular
. {) d \7 S) m) C0 p/ M9 eresponse have included only patients with a good response to imatinib. We
2 ]. o7 |, I1 r4 h' Jdescribe three patients with stable complete molecular response on dasatinib; ~7 |. a. C( e0 V3 F* I, X5 f6 V
treatment following imatinib failure. Two of the three patients remain in- k4 ^; f& q* S4 |
complete molecular response more than 12 months after stopping dasatinib. In
3 C) [8 Y; a* M6 D, ^these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, F1 K8 t' W8 R
show that the leukemic clone remains detectable, as we have previously shown in
4 G, {3 l: e$ A ?# f. b) qimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ m$ G9 f" c- zthe emergence of clonal T cell populations, were observed both in one patient9 }: V- L6 K8 `7 h3 A1 P0 R2 L
who relapsed and in one patient in remission. Our results suggest that the8 p0 G- ^6 I W# D
characteristics of complete molecular response on dasatinib treatment may be8 a _7 W& t; W, g0 a2 p( S, l
similar to that achieved with imatinib, at least in patients with adverse, t. t% ?! V0 |5 q1 z6 ]3 k
disease features.2 G! w- E0 c. w" N' {
|
显身卡
