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。 D+ z* L8 @% @ }6 ~0 `
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。
! v7 e) u/ Y6 J/ [0 a % S; ~* o) V# S6 S
作者:来自澳大利亚$ J) C8 |% J; l
来源:Haematologica. 2011.8.9.
' W$ t$ }) r T- |$ p6 T7 C: WDear Group,1 F6 P4 _1 L3 _: {3 @
2 v# a. M v; n0 o* c; O& z
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
; l+ A1 @3 q" `; b* c4 t+ btherapies. Here is a report from Australia on 3 patients who went off Sprycel' _& U/ b! @$ z7 G# l( d. p% {' v1 Z9 s
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
! L- s" V4 X) Q+ i% C1 Dremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
6 h& D6 ]1 C1 x9 t1 Udoes spike up the immune system so I hope more reports come out on this issue./ Q$ I/ Z' g' V! g: u- ~ [
; Z9 M0 b4 B- EThe remarkable news about Sprycel cessation is that all 3 patients had failed
# K4 M& c( A0 B0 r1 ~5 LGleevec and Sprycel was their second TKI so they had resistant disease. This is
* Z5 g8 o( U/ w5 U: t9 ]different from the stopping Gleevec trial in France which only targets patients$ I% f8 a/ F, y; e$ g; T
who have done well on Gleevec.) X' }) \* j: _+ B+ e% r
4 G) h9 y1 Q5 B, C. e8 x$ `Hopefully, the doctors will report on a larger study and long-term to see if the P8 a. \2 N4 X }
response off Sprycel is sustained.( f! p$ |) ^6 [ x; ~) d: W% O
" o; V) u/ e5 J4 a
Best Wishes,
5 }- a z# T1 \. p% kAnjana J. } t/ [4 D! e2 O" W
% n& C, ]4 Q# |* R
5 V! A8 K: f. N
4 y/ O; z+ _9 n2 A" G
Haematologica. 2011 Aug 9. [Epub ahead of print]
/ w. \6 O6 g8 ?( Y. ?6 n ADurable complete molecular remission of chronic myeloid leukemia following3 E9 r% N/ P. n3 q: r( @
dasatinib cessation, despite adverse disease features.
* P7 s+ Z2 p3 ]+ q8 tRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
2 U7 E8 j* K1 V6 n1 _, FSource
% X' ^8 z% d+ d+ N7 d) ?Adelaide, Australia;
* c3 d9 I0 Q9 |! @* `% H4 g7 z9 Q0 i4 d. l0 b0 T
Abstract. b G% _- ~) l+ |8 F0 {9 k. ]; g& f
Patients with chronic myeloid leukemia, treated with imatinib, who have a
; T3 _. }( Z, `; fdurable complete molecular response might remain in CMR after stopping0 S) w+ Y7 V" J9 [! R) ~0 F1 e
treatment. Previous reports of patients stopping treatment in complete molecular
, ?1 Y( F& }& a- s6 Q0 ?response have included only patients with a good response to imatinib. We( X8 q5 W8 j, y. M9 j5 c U$ a
describe three patients with stable complete molecular response on dasatinib+ o6 W1 A: C: D5 u
treatment following imatinib failure. Two of the three patients remain in
& s3 e5 K1 |' h1 [0 hcomplete molecular response more than 12 months after stopping dasatinib. In4 l8 R# P2 d( a+ C
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to! q7 m; g+ e# F) W X$ K
show that the leukemic clone remains detectable, as we have previously shown in$ `* @, b) w0 _8 g3 z0 n
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
* V$ c0 Q2 R/ G7 H9 A" k: Fthe emergence of clonal T cell populations, were observed both in one patient
$ f) r* p( {- h6 s8 i! ewho relapsed and in one patient in remission. Our results suggest that the8 l9 t z$ U6 X: T5 g) {# ~
characteristics of complete molecular response on dasatinib treatment may be
% u8 [( S2 q* R+ Z. P) t$ n6 Qsimilar to that achieved with imatinib, at least in patients with adverse; J7 [1 n) P3 E
disease features.
1 p% r( \- l) k* n% v; b |