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。
8 d, E3 t) g' x+ O8 h+ r8 i/ X 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。: q# f( ~9 N& c( E
0 p! z6 B# h: |" F* ? V2 s
作者:来自澳大利亚
& I4 r8 z5 ~" Z) E6 e来源:Haematologica. 2011.8.9.) Z" F* U, ~: t- \ \2 u" @
Dear Group,
2 i/ [; J. ~3 u$ R
' A8 m( }$ U2 Q% E# [) P9 DSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
9 Q3 a6 e2 n- Otherapies. Here is a report from Australia on 3 patients who went off Sprycel
7 U# E1 k& F' M+ g0 s4 f0 ^after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
6 V" U! ~( a3 Dremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 s: z2 R/ V5 N7 p9 i5 W7 G' p; q/ ?
does spike up the immune system so I hope more reports come out on this issue.
# ?4 w, N- C; I- Q, ?9 Z0 B8 `+ w% X. m0 k2 J1 K% Y
The remarkable news about Sprycel cessation is that all 3 patients had failed
" Z3 l! o+ c. fGleevec and Sprycel was their second TKI so they had resistant disease. This is: n2 F: m# R$ ^& g9 p* Y" K
different from the stopping Gleevec trial in France which only targets patients+ G" u* K: C. T" x. o& l
who have done well on Gleevec." d1 ~9 d+ o3 g/ M7 R2 b& Q
# Y$ f8 x B. K4 T/ q5 dHopefully, the doctors will report on a larger study and long-term to see if the
2 a2 K* l9 R z% H Jresponse off Sprycel is sustained.
7 O' ^& D4 x+ E1 E: `; ^- Z6 X) X0 q' c# o/ v5 p
Best Wishes,1 p0 M3 Z' R/ Y$ u8 s
Anjana- }3 x, T& z) z. A e
8 D. ^6 t8 Y, ?( b, m- E& j) _. Z8 a. @2 O# l! u
" Z+ _/ {% B: j5 N
Haematologica. 2011 Aug 9. [Epub ahead of print]( Q Y3 s( }. W5 m, N
Durable complete molecular remission of chronic myeloid leukemia following
8 g$ P. m! i0 f8 P9 F; [" W! `; F7 ] wdasatinib cessation, despite adverse disease features.
9 {) m. f' s3 n2 T5 |Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
1 y$ h: d4 F- n3 J, YSource$ H+ Z) Q+ V! L. E2 y3 n" c
Adelaide, Australia;
( h* T" ?+ m$ ~9 y- J7 h% p' \; Y- a! [1 H5 e5 o
Abstract3 c. a9 \* T; L+ L9 V- z
Patients with chronic myeloid leukemia, treated with imatinib, who have a/ }0 n# P/ z" s
durable complete molecular response might remain in CMR after stopping
6 x( j0 p( y+ h. ~1 jtreatment. Previous reports of patients stopping treatment in complete molecular
# r: |) D( j& Zresponse have included only patients with a good response to imatinib. We+ q( {( w. q' f4 Y* `4 |
describe three patients with stable complete molecular response on dasatinib0 F8 s$ E7 _. M0 g& u
treatment following imatinib failure. Two of the three patients remain in
: N# m9 ^ {2 Kcomplete molecular response more than 12 months after stopping dasatinib. In2 w J' M. }) R1 r7 D
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, ^/ m0 Y- w( ~
show that the leukemic clone remains detectable, as we have previously shown in+ a5 j( n+ Z7 a4 v
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as& v" m8 x$ {) o" A3 v9 e4 U1 `
the emergence of clonal T cell populations, were observed both in one patient5 {4 t9 v( N; G) _
who relapsed and in one patient in remission. Our results suggest that the
' W! ]( C$ n) m! V9 Tcharacteristics of complete molecular response on dasatinib treatment may be* y, M! E3 Y) D3 W A- N
similar to that achieved with imatinib, at least in patients with adverse
# y. { a' g+ Adisease features.
5 Z+ @: l4 s0 y! v; _3 @5 \$ a' Z# Z |