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。
" q) B2 z' |5 z' O. C s$ L$ K4 ? 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。5 _4 [- A9 T9 f6 d0 ^) W
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作者:来自澳大利亚, e: ~5 {* {, {. c3 X- u
来源:Haematologica. 2011.8.9.
' Q2 u* Z% t/ i/ W" {1 KDear Group,/ [& R. G6 J9 Y$ u: A0 n
q5 A* t7 g3 nSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
0 m8 x4 N, R5 P1 @5 {- O% xtherapies. Here is a report from Australia on 3 patients who went off Sprycel
# F; {8 A1 s% k% \" A3 H* Y% mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients1 S: P) `/ n! s# L0 p3 Z1 a; l
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- E8 `5 u6 w0 E, f# p. rdoes spike up the immune system so I hope more reports come out on this issue.
+ ?+ C& c: u, m
2 O; F$ a* {4 M, SThe remarkable news about Sprycel cessation is that all 3 patients had failed
: a& V) p/ l! R1 ]0 }9 n6 g" n0 YGleevec and Sprycel was their second TKI so they had resistant disease. This is, @: h8 K, j+ m8 L! F3 Z& g
different from the stopping Gleevec trial in France which only targets patients
+ `0 v! P8 O, L5 g1 H7 lwho have done well on Gleevec.5 r- D5 ?/ ~7 J
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Hopefully, the doctors will report on a larger study and long-term to see if the5 {% U+ J u, K: e( `
response off Sprycel is sustained.9 T0 g! K% p, x* ?8 h f
2 @( G1 x! K# n- ^" N" Q8 i* lBest Wishes,- E; R/ T- m i- |! }& A
Anjana1 \9 g6 `5 d5 g i# `
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Haematologica. 2011 Aug 9. [Epub ahead of print]% v9 y/ u3 N% m% ]/ R* d9 i) E
Durable complete molecular remission of chronic myeloid leukemia following
( p* c J5 q. N# t E& E! l! j B+ [dasatinib cessation, despite adverse disease features.
% ? _* W( a6 `; E# y; PRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
t7 g! A5 r: p+ j* q- TSource
! D0 t, d* a' n$ ?1 p: n* |Adelaide, Australia;
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Abstract8 J0 T! U4 {: d! M0 J. {; o
Patients with chronic myeloid leukemia, treated with imatinib, who have a) m# d' ?& k0 T. B! [( |0 b
durable complete molecular response might remain in CMR after stopping
5 A5 r7 `, a- F2 [) A7 Etreatment. Previous reports of patients stopping treatment in complete molecular
]0 E- v- k$ v8 a3 \- X& \: W7 B4 Jresponse have included only patients with a good response to imatinib. We+ n8 g5 v" F6 R- M
describe three patients with stable complete molecular response on dasatinib
+ b5 ?1 D) ~: q6 H9 u" ztreatment following imatinib failure. Two of the three patients remain in2 Q y+ `) @; e' Q2 d
complete molecular response more than 12 months after stopping dasatinib. In" e; N4 }+ q3 [5 E0 v, \
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to5 ?/ D3 j! r" l! g, Y* ^+ W& E" I, j I2 A
show that the leukemic clone remains detectable, as we have previously shown in1 S& }0 I0 O4 ~2 I
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- O+ K7 f2 d0 b/ ?" v
the emergence of clonal T cell populations, were observed both in one patient
, q: m) ]8 [: J+ _( A9 V9 Uwho relapsed and in one patient in remission. Our results suggest that the8 p, d5 G4 _2 @* O
characteristics of complete molecular response on dasatinib treatment may be
1 u; M/ B% g& T! n- m) ]3 Ksimilar to that achieved with imatinib, at least in patients with adverse
2 b- z0 v5 T, @1 idisease features.7 z3 h* u; T. n) w8 B
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