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。
1 }5 F7 ]( \! t7 ]" } 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。# U7 P% y% y# n& d3 a
% e6 G& G6 t# f6 q0 E% H作者:来自澳大利亚. |# U, r2 J2 p2 V) z' M$ R
来源:Haematologica. 2011.8.9.1 A. n# [: {$ `/ X1 t1 C
Dear Group,3 X4 W, Q* X" z0 z, f( o
* M+ |/ ~6 f v5 {4 u% TSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML x% ?+ b) R/ o3 M2 g# P
therapies. Here is a report from Australia on 3 patients who went off Sprycel+ O% E9 u1 k0 r1 t
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
, ]4 A, I" X7 a' i M- W4 P+ premain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# G( M2 F$ ]5 D3 U8 t& \7 H8 h/ Mdoes spike up the immune system so I hope more reports come out on this issue.
5 P9 L [) @& n# M. L% T& S q& v- J) M0 J- Z
The remarkable news about Sprycel cessation is that all 3 patients had failed4 J; Q/ o- q9 ]$ ?3 r
Gleevec and Sprycel was their second TKI so they had resistant disease. This is' E& {7 w, Y7 t. s: Q. M* O
different from the stopping Gleevec trial in France which only targets patients' z _2 K6 W O A$ x
who have done well on Gleevec.
( Z( v6 w6 q( p% H S( ~1 ?* `# L$ i6 `* h. P
Hopefully, the doctors will report on a larger study and long-term to see if the
2 c" W7 m# A) Q- [6 u$ b# cresponse off Sprycel is sustained.# E# D: t. I& u) ~9 _
. U' _5 t: @" c5 _% u* i
Best Wishes,
0 C' h" y) J' k# n! ^0 NAnjana5 y+ j! x7 Y; a
7 E* e3 p- o5 J0 @2 f
B0 i' g3 q& b( ~! g5 Y5 B
; \) ~4 c) T+ J T: x3 gHaematologica. 2011 Aug 9. [Epub ahead of print]9 f9 k: |7 ?# K8 | s# ]
Durable complete molecular remission of chronic myeloid leukemia following$ u0 }5 c& y1 A
dasatinib cessation, despite adverse disease features.
* A- G4 w9 m! N* BRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.0 f) P# ~2 H! y; E) e) T a
Source
X7 I' @0 R& V, X: N' UAdelaide, Australia;" K) a; m. [4 {( h
; X* V3 i( C+ SAbstract) W8 ~) j4 r0 k
Patients with chronic myeloid leukemia, treated with imatinib, who have a# O0 \1 B2 @+ l" V
durable complete molecular response might remain in CMR after stopping
1 ?' M- U- X* K4 ^' v8 ~& utreatment. Previous reports of patients stopping treatment in complete molecular
& e3 T) e7 v Q$ F s) Lresponse have included only patients with a good response to imatinib. We
& F2 u0 R- C0 o- C8 d8 I7 \- ~+ edescribe three patients with stable complete molecular response on dasatinib
9 W, t# F, _1 @2 @+ |( E8 `/ btreatment following imatinib failure. Two of the three patients remain in, a! U9 }7 c; B+ Y: O) u1 T
complete molecular response more than 12 months after stopping dasatinib. In% ~- x$ s2 {9 }, w# X1 `8 S
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
) b: H, x" o. W7 y- }# Jshow that the leukemic clone remains detectable, as we have previously shown in7 @9 B( @$ _5 s
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as, G' K1 R* A! |' G* m2 [8 f
the emergence of clonal T cell populations, were observed both in one patient* V6 }9 h! x9 h
who relapsed and in one patient in remission. Our results suggest that the& _& v( C4 g5 H5 q' k
characteristics of complete molecular response on dasatinib treatment may be1 | O, g* z* |7 T5 N
similar to that achieved with imatinib, at least in patients with adverse4 Z. k( m3 N4 H' B- J8 s
disease features.1 J# C# H+ O1 i! z5 S
|