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。
, E8 i" s+ R3 Q9 }7 t) H 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。
0 h! m4 v3 X5 {- P - O5 h7 [8 v1 {. o3 I+ P
作者:来自澳大利亚
z3 ^0 q) D+ H来源:Haematologica. 2011.8.9.
! z% \$ f3 o5 r5 Z! i1 FDear Group,$ ^* ?: @1 J p K* m* m. ]6 ]! s
5 Z9 R4 D4 `+ u, `! hSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 Y# ]9 H# F& I9 i+ v- J
therapies. Here is a report from Australia on 3 patients who went off Sprycel0 C% A- o0 I/ o: @( [& w* l# W9 `
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
( M V# }* i6 W2 jremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
5 [# q' {, I' H2 |2 Ddoes spike up the immune system so I hope more reports come out on this issue.1 ?, \3 }/ Y4 C6 h2 _8 g
$ |9 U* P$ d% G) W# o2 X
The remarkable news about Sprycel cessation is that all 3 patients had failed
, q: b: b- U [4 o# v* L$ G5 UGleevec and Sprycel was their second TKI so they had resistant disease. This is7 x y. m( |" L* N$ I" u0 b
different from the stopping Gleevec trial in France which only targets patients
! }+ y& r% t5 n, f4 E# e2 }5 ^who have done well on Gleevec.) V7 u8 |. `9 y0 q% y0 f
6 U* F* G& D6 r3 i$ j c+ IHopefully, the doctors will report on a larger study and long-term to see if the
+ t7 j2 T% y" h3 r, |! Dresponse off Sprycel is sustained.
/ d; E7 L/ o, k' y4 g
4 T$ R7 M5 {, b6 Y, F% F0 hBest Wishes,
x/ @+ E# O8 X$ x% e- AAnjana
3 ^" U9 M; w# W; Z3 q0 r( A
1 o3 I( p) x; P. Z. R4 ^/ {* { P9 Q5 T9 b( J F1 @$ a% O
) f! e$ ` a2 H- s, l; K% pHaematologica. 2011 Aug 9. [Epub ahead of print]$ D6 p$ ^- O; f, F* D
Durable complete molecular remission of chronic myeloid leukemia following' x |! [1 U7 ]8 _& \3 C4 }
dasatinib cessation, despite adverse disease features.
+ L7 J* [; z/ D: oRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.8 P, d; R! I3 w L, ?
Source
8 |( F( R- u/ _$ GAdelaide, Australia;
8 Y+ k- @+ H$ b K @
* J0 o, U: N! ~, i2 I* FAbstract
1 I; X* v* _' vPatients with chronic myeloid leukemia, treated with imatinib, who have a0 u" x1 G0 @" a) \
durable complete molecular response might remain in CMR after stopping
{7 l6 v* k# j, Z4 U8 |0 Jtreatment. Previous reports of patients stopping treatment in complete molecular
7 L) P' L* ?1 F, \" Q7 o/ O4 Tresponse have included only patients with a good response to imatinib. We) ^# z" y" J& V9 u2 o2 H
describe three patients with stable complete molecular response on dasatinib; ^* `4 a+ k- V- d8 a
treatment following imatinib failure. Two of the three patients remain in! u' }( d/ ?# K. s6 P
complete molecular response more than 12 months after stopping dasatinib. In; ]2 H" w( [: g; O# v
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* u" U/ f6 ?/ c8 Gshow that the leukemic clone remains detectable, as we have previously shown in$ a" W6 L# V6 q& E% z `
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
: n4 a4 \3 Y0 e. U. r, C4 pthe emergence of clonal T cell populations, were observed both in one patient0 r# u& R# k" `7 ]
who relapsed and in one patient in remission. Our results suggest that the
- W H8 a6 s, C0 \3 N; i. {characteristics of complete molecular response on dasatinib treatment may be# i9 e5 h% j: F7 \2 ]
similar to that achieved with imatinib, at least in patients with adverse* w5 M/ T" r0 ^$ l% t+ O
disease features./ a+ [4 i+ q; V8 m
|