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。
/ g" f$ v# H: I! a. M 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。( n3 P0 n3 w0 m
/ g! w' q, I& Q) }: f作者:来自澳大利亚 e# S5 s4 p- l8 O5 p! C- i
来源:Haematologica. 2011.8.9.0 ? [0 K( _+ E+ y: l! ~3 O
Dear Group," S% k- G* c# u" E$ H8 U5 t
) B; l! \) o) v1 \9 ~. iSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
- E! g* V* o9 P; G$ s6 {+ M! Etherapies. Here is a report from Australia on 3 patients who went off Sprycel
8 N" l9 q2 {' u6 Bafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
4 r6 P2 B9 ?8 Q- [% eremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel. ]8 W- |( \$ W4 b* a3 `* n
does spike up the immune system so I hope more reports come out on this issue.4 q$ S" G' a- K9 Z9 H
8 J5 g6 Y% g. L3 Y& f1 y; |The remarkable news about Sprycel cessation is that all 3 patients had failed9 p8 l) f, h" m. f/ e" w% t
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 @) h6 F, D5 p2 D
different from the stopping Gleevec trial in France which only targets patients
3 ^+ G- q% X8 Y% w( n' w+ n# kwho have done well on Gleevec.
6 F( u, j! A- J( q% ]; u
$ {2 `# G" D6 s I" p6 k& rHopefully, the doctors will report on a larger study and long-term to see if the( w, M s- t: H
response off Sprycel is sustained.9 }9 b, o2 t. L
0 P8 I; p2 A" a' X! H# B7 W+ |
Best Wishes," w" q% B) X( u& z, F
Anjana
) |3 H) \% S7 m b) T V! L
2 g4 E! H, v% f* z7 z% p
4 R% ~+ z0 C3 q# @3 W/ X; l
) l( l9 H$ y& K4 V. d6 qHaematologica. 2011 Aug 9. [Epub ahead of print]) z. M! e& K$ k x3 o/ y3 W& n: d- u
Durable complete molecular remission of chronic myeloid leukemia following. I( A; F! g# g5 h) Q0 W
dasatinib cessation, despite adverse disease features.( Q# P! Q; Y- }
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.3 h/ M- l' e, c
Source
7 Y$ {) L# O$ \1 r1 |Adelaide, Australia;
3 ~7 [0 {) {1 G, b' r
K$ h2 G8 Q; c. ^2 G+ I! o4 iAbstract# Y, l- k _2 [/ u* G7 A) ]
Patients with chronic myeloid leukemia, treated with imatinib, who have a
1 n/ w+ z, ]2 L0 g0 vdurable complete molecular response might remain in CMR after stopping
1 j4 q: Y+ @' {6 q: Ntreatment. Previous reports of patients stopping treatment in complete molecular
/ Z4 B7 c# j1 c) T( @response have included only patients with a good response to imatinib. We7 C# [7 S6 H5 j3 R) @
describe three patients with stable complete molecular response on dasatinib" H4 l# L8 k4 t* a( r, v4 x) |
treatment following imatinib failure. Two of the three patients remain in" |5 x. P9 v! P2 t; \
complete molecular response more than 12 months after stopping dasatinib. In
3 ^5 \5 D! q0 fthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to1 F) e/ V- P* g
show that the leukemic clone remains detectable, as we have previously shown in6 }: _+ `' f' s- n# h3 W
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as, \4 U: n8 |) j
the emergence of clonal T cell populations, were observed both in one patient
% X1 s8 f4 _% i& Ewho relapsed and in one patient in remission. Our results suggest that the. z$ H3 k5 z6 R" l/ q
characteristics of complete molecular response on dasatinib treatment may be. p6 p5 t% e5 I- ?% ?6 ], o
similar to that achieved with imatinib, at least in patients with adverse( U% m3 F$ ^& L( }
disease features.
! K. I$ r& d: p! n1 E4 C+ P |