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。, ~. F# O' k6 @5 J" ~3 R7 C& l
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。/ d' I" V" m) |- _: s$ c* W6 v
7 B" K0 F/ q& }2 T作者:来自澳大利亚- M$ h, B2 C" w* C
来源:Haematologica. 2011.8.9.
) h' ]" ^' b$ gDear Group,) D; I4 ^: _( ^: W8 d% V3 ?
7 G8 S( e. i l u, \: ESome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
1 e( h8 x& O4 D. a, m, B1 ~therapies. Here is a report from Australia on 3 patients who went off Sprycel
9 s& t: S6 ?" W: r8 Mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
" L% R1 ?' U3 u; e) [" E$ l9 Tremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
4 I. E2 I/ E+ T7 [3 w9 Wdoes spike up the immune system so I hope more reports come out on this issue. I" G; k1 o# e' K+ w3 o
1 {: X& j/ T1 s# H8 Q) d( GThe remarkable news about Sprycel cessation is that all 3 patients had failed9 i2 b9 E0 D9 c7 |4 Y( b$ k, E
Gleevec and Sprycel was their second TKI so they had resistant disease. This is3 m. p7 b d# k3 Z. x4 H
different from the stopping Gleevec trial in France which only targets patients
. c. [/ A6 [, n Hwho have done well on Gleevec.
4 t0 a9 q* O! z& F6 R# t8 Y- K7 l- @3 \0 J5 g7 v
Hopefully, the doctors will report on a larger study and long-term to see if the
' Y. z7 t, s2 E1 C/ @/ g. {response off Sprycel is sustained.
, g( ?6 n5 L4 \* i0 o# F
5 A& B) R7 w. t/ ^8 L4 H) zBest Wishes,
5 P- X9 K% p/ j: ^, B% ~2 \Anjana
( E1 [2 W8 c; L0 |% y
' l- a: Q, y4 o: Q' ^/ k+ q8 n* o( G, L: I7 j4 v" a
3 J5 ~% R' s, K4 v; QHaematologica. 2011 Aug 9. [Epub ahead of print]) W9 z9 Q8 r0 G) i
Durable complete molecular remission of chronic myeloid leukemia following
6 t% E+ p) ^5 Z1 zdasatinib cessation, despite adverse disease features.. |. T" i& F" V5 } R# P
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ p( F7 s& a2 j: @
Source
* J3 n$ S% i, ^( i* L6 f3 r& z+ vAdelaide, Australia;' {2 b' b, k* v% w" b* o n0 u
' D- R& F" e1 B- G u
Abstract) m9 q5 I! ]+ N4 K1 p6 _
Patients with chronic myeloid leukemia, treated with imatinib, who have a0 l+ K4 N2 _! S9 s0 f
durable complete molecular response might remain in CMR after stopping
! f4 D6 q! B6 ^5 G: W: Itreatment. Previous reports of patients stopping treatment in complete molecular( ?( l. x7 \, b6 J% \
response have included only patients with a good response to imatinib. We/ q/ q8 b3 R/ X/ c
describe three patients with stable complete molecular response on dasatinib, @# ]5 Z I5 \2 k; Q
treatment following imatinib failure. Two of the three patients remain in* H4 i- u6 t' y1 z
complete molecular response more than 12 months after stopping dasatinib. In; W1 H2 @/ Z1 e# g0 y6 h
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
( T" c- ^% y$ j4 |2 cshow that the leukemic clone remains detectable, as we have previously shown in
4 K. `" e, k, X& Ximatinib-treated patients. Dasatinib-associated immunological phenomena, such as
( x& Q9 E- h& }1 @0 r- jthe emergence of clonal T cell populations, were observed both in one patient
/ Z9 t9 h e9 k2 Y: Iwho relapsed and in one patient in remission. Our results suggest that the% C) g4 O8 {! L1 f
characteristics of complete molecular response on dasatinib treatment may be3 I+ s3 r5 S0 @7 @) M# ~2 A
similar to that achieved with imatinib, at least in patients with adverse
; A% G; L! |7 L6 p* O" {disease features.
: j& r. |- C( E, S |