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。( E b$ w) x6 o) M" F- I
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。/ _1 G& D$ K/ O# n+ ?
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作者:来自澳大利亚
* H# O$ z3 P: l% w: W2 I" B来源:Haematologica. 2011.8.9.% e; D# x. ^; Q
Dear Group,9 L3 G) u/ v3 I [8 ~+ b
9 @7 f& r4 c+ I0 k0 oSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
k6 d2 f+ C+ K7 N$ k4 P, F: j# \therapies. Here is a report from Australia on 3 patients who went off Sprycel
, D; g$ x' t6 E- A# \' u$ uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
2 `% b, D. `- R6 D& r8 xremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( j2 M+ ~& S6 b) ~% n
does spike up the immune system so I hope more reports come out on this issue.
/ A: R( S) u% U- ? n& |$ `, a
8 \. f* X# ~/ b3 l3 E0 E! BThe remarkable news about Sprycel cessation is that all 3 patients had failed
3 p: v' |5 b# a) }9 _# NGleevec and Sprycel was their second TKI so they had resistant disease. This is
& ]- _0 x5 G6 }( i' Ldifferent from the stopping Gleevec trial in France which only targets patients* ~% d- t3 N0 B: `+ _- k3 a0 w5 y1 d
who have done well on Gleevec.
7 u, _$ I# X) _- ?) H& v
7 y& Z; g- f# Z/ v" j3 CHopefully, the doctors will report on a larger study and long-term to see if the; J2 }5 W0 o, X
response off Sprycel is sustained.
; q% A2 ?' f3 b& I0 B( `( C; u2 c3 u0 v# k% X
Best Wishes,
. v5 R" F) _9 k, w" |! P; {& IAnjana
; }+ S, V& W/ [; k6 m+ u. y
: R1 V! u. W- @9 k/ Q. s
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Haematologica. 2011 Aug 9. [Epub ahead of print]
" E; k4 g5 N8 } n; O4 @Durable complete molecular remission of chronic myeloid leukemia following
6 B( T# ~8 F0 l& Jdasatinib cessation, despite adverse disease features.
7 q1 a" {) h' S3 ?$ M* X* {0 {+ p& gRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.$ x6 b, v2 l. @9 l" Y6 O
Source
$ g: c2 |: v1 J9 D/ xAdelaide, Australia;) w, T# ^) d' x( f! M( r3 z9 H
q9 Z. ]& H& n) x) RAbstract
( A- J( a$ E: \# p# Y! A: }Patients with chronic myeloid leukemia, treated with imatinib, who have a
+ s. \& h' o+ x. r; Gdurable complete molecular response might remain in CMR after stopping
+ H+ h- D4 w2 C' W4 C/ n9 A1 H3 [7 ~treatment. Previous reports of patients stopping treatment in complete molecular
! b w+ A) F2 ~% F' n! o7 T4 _response have included only patients with a good response to imatinib. We; \: E1 ^4 t" M% _& i' e
describe three patients with stable complete molecular response on dasatinib$ V2 I5 x2 s, y# P
treatment following imatinib failure. Two of the three patients remain in0 f5 ?' V1 S# J- n# X
complete molecular response more than 12 months after stopping dasatinib. In- N k" `$ k/ D! T z" h
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to( Q8 k) `/ ~5 L% {* ]
show that the leukemic clone remains detectable, as we have previously shown in
0 H/ R7 b3 i3 G5 Wimatinib-treated patients. Dasatinib-associated immunological phenomena, such as5 v' `" ^+ ^* G
the emergence of clonal T cell populations, were observed both in one patient7 I5 T! t* P) p4 x7 t
who relapsed and in one patient in remission. Our results suggest that the3 ?6 C1 X) N" `: v) Z
characteristics of complete molecular response on dasatinib treatment may be
# `2 V" [: ?0 B4 Hsimilar to that achieved with imatinib, at least in patients with adverse9 V5 Y( s, z7 o1 \$ r; r! i5 D
disease features.) d {5 n2 n- l
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