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。
: A {1 p' c" Q% l 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。) V" ?8 L+ M! E4 `- W: Q
, k, w( [0 n* Y& E( F) a% N
作者：来自澳大利亚$ S' w `, ^' t
来源：Haematologica. 2011.8.9.
; E, p! i4 P4 i+ M g" YDear Group,# }& |; c/ P( p1 _
U0 b' ~! k3 P% B7 fSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML) j) G% X$ }& _6 A4 A% c: U
therapies. Here is a report from Australia on 3 patients who went off Sprycel
+ O) a5 a% o! C) l9 d- wafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients% ~$ A; ^7 x1 P# ` [0 E0 u
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel* o( y' _. b) c, B
does spike up the immune system so I hope more reports come out on this issue.
1 J* V% b0 {+ W) L6 g0 b3 w" z; J. j
The remarkable news about Sprycel cessation is that all 3 patients had failed- ^+ m- E4 F8 S# Z# |! Z
Gleevec and Sprycel was their second TKI so they had resistant disease. This is- _5 o+ F# Q/ n7 m
different from the stopping Gleevec trial in France which only targets patients
% Y- `5 |$ M' A. f1 \: m/ [7 U4 v9 kwho have done well on Gleevec.
# K0 M: h; S7 l) ?7 S& m' e9 I/ E
; H% q! s5 T$ i% x1 M6 w7 H! `Hopefully, the doctors will report on a larger study and long-term to see if the
: R: S1 |1 V. Y* i$ mresponse off Sprycel is sustained.
, c' u3 d2 `& o G# s# e6 m
" L& a6 W! [; x9 h$ dBest Wishes,
3 R# L- P q) A/ lAnjana
: n5 K4 i( K* H! u. b% Z. ]/ p; f; m# }( ]
( I+ g: e) N s" S; q- G/ d
$ Z8 Q, D# O; q6 t
Haematologica. 2011 Aug 9. [Epub ahead of print]
' U7 |( ]/ U u. p$ F# LDurable complete molecular remission of chronic myeloid leukemia following
& c' `4 U. }6 D% t* x" s) Hdasatinib cessation, despite adverse disease features.
% \% i1 _; P. S( {' A/ R5 {Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' u" |, I: b; W3 ~
Source5 l2 L3 X- ^. j" W ~
Adelaide, Australia;8 o( W" [( e" j! w5 A( M& Y
+ m8 @ D7 z- h4 YAbstract
; W) t2 I7 f7 JPatients with chronic myeloid leukemia, treated with imatinib, who have a8 O; U, S" n9 }$ k7 N/ B, p
durable complete molecular response might remain in CMR after stopping
4 k, i+ D( E: N/ S" n8 Z. \treatment. Previous reports of patients stopping treatment in complete molecular9 o! g2 W% p3 Y5 [. b& d
response have included only patients with a good response to imatinib. We" |! }, E3 j; h: @8 p
describe three patients with stable complete molecular response on dasatinib
) e3 |9 Q+ G, W- p0 P4 dtreatment following imatinib failure. Two of the three patients remain in
, A6 P1 q8 W& b" {complete molecular response more than 12 months after stopping dasatinib. In
, `* X+ F4 {7 d- w0 N2 g- t4 i$ |these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to' N9 ] z: q( L' k" {
show that the leukemic clone remains detectable, as we have previously shown in
! R- b2 d4 ?0 Z7 y3 X! T; Rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
9 }3 `( Y* `# a+ b7 ~& X+ c! }the emergence of clonal T cell populations, were observed both in one patient. ]5 ~+ `7 E( E& Q. s
who relapsed and in one patient in remission. Our results suggest that the
* A4 H9 k$ i5 z# Z. q2 [7 |characteristics of complete molecular response on dasatinib treatment may be5 g# Z; U& h) b/ i; @7 Y. {6 f
similar to that achieved with imatinib, at least in patients with adverse
9 f! I1 I& J. q7 rdisease features.
! d; D, X n2 ^3 \0 o" ], W |
显身卡
