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。
( i+ g! M+ I: G. q6 ^) h4 I* q! r 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。
$ Y d; ?+ ?+ f# x 1 F- ~; |1 c, L! P; Y# C' n% m
作者:来自澳大利亚" u* V) N# n K2 g; S* s
来源:Haematologica. 2011.8.9.
! B& B, r3 A: T! T+ ADear Group,
8 A- h: F/ w" K% r4 I3 G0 H4 _5 c
. [; k4 f& e) ^7 vSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
& F+ c. p% [7 f( e+ u5 [9 w8 Ntherapies. Here is a report from Australia on 3 patients who went off Sprycel
, y9 N* E9 `% K/ pafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
9 R. y1 C' W# Xremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel0 L4 i" U. S- G
does spike up the immune system so I hope more reports come out on this issue.# A- j, Z* D# \( ^8 b
$ \" V' m4 ?) @ U. v, T' ^
The remarkable news about Sprycel cessation is that all 3 patients had failed
6 ~& X7 U: l+ z) G2 l0 f7 wGleevec and Sprycel was their second TKI so they had resistant disease. This is
0 N1 ]8 R4 T3 w+ Kdifferent from the stopping Gleevec trial in France which only targets patients
0 c# L( @+ h+ s+ ]0 |who have done well on Gleevec.
+ Z. Q& S- N# K% E2 t. v
5 b/ E7 ]; B# I$ g) n; |Hopefully, the doctors will report on a larger study and long-term to see if the- c6 l- @% i5 v& j7 Z
response off Sprycel is sustained.( C3 L6 ?. H* l+ A. V( k4 q
- ^( _- X q4 HBest Wishes,5 P! D, Z1 O4 \" \$ A4 j+ a2 ~9 W
Anjana, O; T6 R" ]" H! T- Y8 Y
$ w9 G2 m- j# e+ K3 _& x
1 _: c3 q7 V& E( j
' c- A6 v( q4 S
Haematologica. 2011 Aug 9. [Epub ahead of print]
. M* g p, A7 GDurable complete molecular remission of chronic myeloid leukemia following5 }2 Z. D/ o( K# d3 [
dasatinib cessation, despite adverse disease features.
) s& N, q& F9 G$ c9 z: g$ A# m1 wRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.5 H a( \, z3 F. y0 v) O
Source
& o. }9 L4 ~# v g( O) ~Adelaide, Australia;' {! m* s; j& W' N: I: l
) K4 E" F+ N# qAbstract
3 M$ E9 E, \3 p4 x* b# }2 UPatients with chronic myeloid leukemia, treated with imatinib, who have a
) d) L: a. W3 h& l$ F9 T$ pdurable complete molecular response might remain in CMR after stopping
6 w. k) m6 ~+ t, A v* s! b4 k! ~treatment. Previous reports of patients stopping treatment in complete molecular
. Q1 @) g8 m+ w7 v8 `9 F) Z) sresponse have included only patients with a good response to imatinib. We4 `3 Z; V6 Y5 w; Z Q* K% k
describe three patients with stable complete molecular response on dasatinib
) S# H& v) U# a. @- H% g) W. Etreatment following imatinib failure. Two of the three patients remain in2 ^9 P! M0 [4 D
complete molecular response more than 12 months after stopping dasatinib. In
p, |; L( b- ^+ C- qthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to( f3 Y* ?/ s: o, j* n0 R' F
show that the leukemic clone remains detectable, as we have previously shown in
7 s* R [' c$ H& ^# Bimatinib-treated patients. Dasatinib-associated immunological phenomena, such as: X. b4 m* m0 k; L# g5 v; m, I
the emergence of clonal T cell populations, were observed both in one patient/ u. B. X4 C$ T! M3 W( S; r* Q
who relapsed and in one patient in remission. Our results suggest that the
1 {+ I; R$ q8 kcharacteristics of complete molecular response on dasatinib treatment may be
3 R* h" [5 \/ E+ Ssimilar to that achieved with imatinib, at least in patients with adverse
1 Q7 p9 v0 S- t! ?& x* bdisease features.
% l/ H1 J7 x+ a6 W3 k, g |