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。
& E7 S* v% P! n8 T 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。0 k( ^5 u1 d7 A- h! ?
% @" ]; f# w% E: g0 ?& X0 C作者：来自澳大利亚9 Z8 T: \6 M s- k8 K
来源：Haematologica. 2011.8.9.. n7 u( G( O" F; l' g. G j' S
Dear Group,. x: f/ n8 W; k4 j$ C( v
+ o4 b: v1 f2 G5 n' qSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
+ K2 |( Q g2 T1 `2 }therapies. Here is a report from Australia on 3 patients who went off Sprycel
! O l0 P- ~2 w+ }; O* ^# r5 iafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients4 S8 B* b4 p0 m* T; g* `
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# w- K) {, E. r) ddoes spike up the immune system so I hope more reports come out on this issue.! k* P5 I* Z% H' ?& ~
& U1 h! }7 ~: `1 G+ Z8 SThe remarkable news about Sprycel cessation is that all 3 patients had failed
- w+ z4 w% L( p& ]/ _0 j/ J" h# LGleevec and Sprycel was their second TKI so they had resistant disease. This is0 Z$ c. a" t' G- E* \5 `: {
different from the stopping Gleevec trial in France which only targets patients
! L, A8 I7 L: L0 C# J9 Vwho have done well on Gleevec.
9 g: j1 K' m) V* T* s2 i. O; K: b' A- ~; o8 F5 x: q
Hopefully, the doctors will report on a larger study and long-term to see if the
% I/ A0 Y+ E- D+ B8 E. Sresponse off Sprycel is sustained.6 \8 V8 X$ V" |1 G( e
. u" a- Q8 d1 i: O2 i9 s7 LBest Wishes,
, G l% f/ F4 s* h0 B- d5 X% GAnjana" p7 W9 V$ @- F: S$ B
& |9 V D" P1 c" l$ g' ~/ K
3 L* L' v) C5 |) S
) w; o- P5 e- G4 G) _/ }' F; `9 [0 ?! CHaematologica. 2011 Aug 9. [Epub ahead of print]0 p( W1 S" z: F ^# u7 x
Durable complete molecular remission of chronic myeloid leukemia following
) E; a" r v, D {- Q$ Sdasatinib cessation, despite adverse disease features.- M! c7 l# n* a
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.) f$ W( c9 ~4 U! B1 M& Y( n
Source
4 q9 O# @& b) {5 H; ~Adelaide, Australia;% t0 I: J) U8 o. u, I! N V6 `* H
) V& B: J$ H, p E; J; gAbstract8 O0 P2 h! s8 ?8 |2 P1 I
Patients with chronic myeloid leukemia, treated with imatinib, who have a' \' q+ A/ \' V7 X1 m' v6 E! T
durable complete molecular response might remain in CMR after stopping
# V/ q6 A6 \# E8 itreatment. Previous reports of patients stopping treatment in complete molecular$ ~% @. u7 r+ d3 c
response have included only patients with a good response to imatinib. We1 a# j) d6 P& j0 i
describe three patients with stable complete molecular response on dasatinib" k- G0 ~2 p( W5 `: _( @1 _! s7 P
treatment following imatinib failure. Two of the three patients remain in* [5 w' v+ u) i8 x6 `: r
complete molecular response more than 12 months after stopping dasatinib. In% J0 u& S$ u! L* [1 k3 y0 _& P5 a
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
% I. x/ a, g" ushow that the leukemic clone remains detectable, as we have previously shown in( N" K' ]5 ]; P8 \2 u5 K. V' }
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as4 f5 y: ?1 K9 M2 K# D. T k- V+ h, H5 t
the emergence of clonal T cell populations, were observed both in one patient
1 k# F2 ]/ y, kwho relapsed and in one patient in remission. Our results suggest that the
n! c' z, N; ?. ~characteristics of complete molecular response on dasatinib treatment may be7 l6 [; ^( X7 l" ?
similar to that achieved with imatinib, at least in patients with adverse
3 G- z0 C4 I' q; G9 S' ^6 idisease features.; k( C0 \3 M- p$ o' E" ~# C
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