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。- G$ I6 D4 d$ O" u" \' X& h
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。
2 ] [4 ^$ D7 X2 B4 c5 B
! Y: o! o/ l& Q% C( ]作者:来自澳大利亚
3 r) L; h& R3 p( g: z$ ]! Q6 k来源:Haematologica. 2011.8.9.
k2 y' s7 K$ i# j! S; gDear Group,! _! R" w4 }* h" v9 X1 H- ]
2 h! {) `! G4 H5 B: Q" G: ]& D( cSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML% ^3 R$ b: n _; K+ X' u
therapies. Here is a report from Australia on 3 patients who went off Sprycel+ u$ n, {5 N2 f% F ?% L
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients0 A) p$ ~! y% f" B
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel( R/ A( U: S2 P
does spike up the immune system so I hope more reports come out on this issue.. e/ Q6 f3 U. q/ a) c6 C/ ^2 y
( A5 N/ [+ @. I% G& N3 v3 O
The remarkable news about Sprycel cessation is that all 3 patients had failed6 Z' L3 j. q. ]! y- D
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 C8 N i& o/ w& c, |# f
different from the stopping Gleevec trial in France which only targets patients5 U! X" ^$ {8 S+ ~5 _
who have done well on Gleevec.
' V2 V- ~0 w" x+ L
, a0 ?- B( i9 J2 ~" U5 P6 F7 B. }Hopefully, the doctors will report on a larger study and long-term to see if the4 Z3 n8 a0 C+ W) U# J. w4 H$ B
response off Sprycel is sustained.4 Z. U1 _3 A6 M0 o4 s
: q, ~0 e& \0 V# l6 D! @$ \
Best Wishes,
, Q4 y( k; P0 M" Q3 cAnjana4 e7 N1 Y4 ^# ^1 V8 g/ i P
9 M7 P: k O% J r0 ^6 L4 @- `/ |3 t
5 f8 R2 r7 V9 h
Haematologica. 2011 Aug 9. [Epub ahead of print]
G' R7 ~3 g4 F p: }$ mDurable complete molecular remission of chronic myeloid leukemia following# z4 l8 E) ~1 w0 s% F
dasatinib cessation, despite adverse disease features.
: B# T/ t" k- o" C& jRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.: ]0 Z' A4 m8 `
Source8 Q1 j- \( X3 t5 C) j2 G6 I
Adelaide, Australia;4 f( Y# x6 G' c' l+ k9 @7 V- w
+ \5 f. a" N+ T {! |( Y3 i: d& O
Abstract
; B1 `- R4 x$ K# ]; [9 u& A' TPatients with chronic myeloid leukemia, treated with imatinib, who have a
d6 c+ Q$ O4 O2 Ndurable complete molecular response might remain in CMR after stopping. o0 h' g" x- V
treatment. Previous reports of patients stopping treatment in complete molecular
3 w3 L4 ?5 F; i% I' R; y* U1 wresponse have included only patients with a good response to imatinib. We& |1 e0 d/ n) Y0 u( M; B
describe three patients with stable complete molecular response on dasatinib
5 X2 W2 T8 `9 ]. Itreatment following imatinib failure. Two of the three patients remain in
4 ~. k$ I* T) n3 @6 m7 {& hcomplete molecular response more than 12 months after stopping dasatinib. In& ?3 b: o) F6 K- _
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
3 U; O* s9 v: C" |" Jshow that the leukemic clone remains detectable, as we have previously shown in
. D" A% a, x! L' aimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
( R t2 ?+ g8 {8 G. \) |the emergence of clonal T cell populations, were observed both in one patient6 k0 O9 v! U9 {! L! Y; `1 O$ M
who relapsed and in one patient in remission. Our results suggest that the( |7 k) s. \+ r
characteristics of complete molecular response on dasatinib treatment may be0 G$ R+ f" A$ J
similar to that achieved with imatinib, at least in patients with adverse
0 t d+ i& H4 L) y+ K$ udisease features.1 F6 e1 i" Z1 @5 u7 v/ Q
|