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。1 J7 \: Y1 `* }1 j
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。
( Z, h! @* [! O% }2 T- r: F
9 K; `) _2 g( {0 x' \. r& a% Z, A$ U作者:来自澳大利亚
7 O" u( u1 p; w" K; a! ~5 X来源:Haematologica. 2011.8.9.
+ S6 b$ {6 q( q% ]: g3 lDear Group,
* g) i7 O9 Z$ g x9 W: q
9 C5 {9 I: U( ? GSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML; V8 q. Y" Q7 T5 l' W7 J
therapies. Here is a report from Australia on 3 patients who went off Sprycel/ K' T8 R* Z# p
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
! i. Y; v4 W& X2 B8 ?0 Dremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel; U D% j- t* n% E, T6 Z% A, R
does spike up the immune system so I hope more reports come out on this issue.& l, ]9 @/ Y. b- \" U8 M
6 Y" Q2 W6 q/ D/ N* b6 p, FThe remarkable news about Sprycel cessation is that all 3 patients had failed- q8 t+ I0 f$ R' x5 \" M# l
Gleevec and Sprycel was their second TKI so they had resistant disease. This is! ]# R* p H! s7 K* R/ L) y
different from the stopping Gleevec trial in France which only targets patients
$ q4 E% u5 V1 ]4 o' s6 cwho have done well on Gleevec.
% C' M9 O, t' A5 e3 S/ I. p+ @4 [4 h1 A- X7 }
Hopefully, the doctors will report on a larger study and long-term to see if the
6 L9 A; \' u# J- s7 x1 i% rresponse off Sprycel is sustained.
, ~) Y0 I' c" G3 V/ X* k) j( E4 a4 ^" s6 z* I+ k# h0 X
Best Wishes,4 y1 Z O( v D3 L/ z# R' y
Anjana D/ Y1 S8 l+ V" E3 Z' S
- R: b! |; y3 @; O7 x; R5 X" m/ O7 X; P* j, y/ Q0 O
4 l S0 |. T( g VHaematologica. 2011 Aug 9. [Epub ahead of print]7 m9 l* ?% V& _" ?* v
Durable complete molecular remission of chronic myeloid leukemia following- j9 m5 `% Z- {0 E: t, O
dasatinib cessation, despite adverse disease features.
( d z4 K( s3 H, S, O2 n! c g hRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( Z& p$ T, w& l
Source9 d- k1 q5 E& w
Adelaide, Australia;
- w1 _7 q5 }' R: |4 y- \5 z- e2 f, ~3 _
Abstract
. |4 [4 M! q1 @' C: s& O) ZPatients with chronic myeloid leukemia, treated with imatinib, who have a/ m1 Q. {3 W# x4 V! Q% s) g" d
durable complete molecular response might remain in CMR after stopping% y5 @# g2 t4 a1 \+ @
treatment. Previous reports of patients stopping treatment in complete molecular5 u$ d9 N& c/ N5 p- c; q9 L
response have included only patients with a good response to imatinib. We/ n* }2 i3 s, p. ]
describe three patients with stable complete molecular response on dasatinib% E- K/ a& i1 m# X" z
treatment following imatinib failure. Two of the three patients remain in6 P" p1 P4 R, k) h+ g- u6 F
complete molecular response more than 12 months after stopping dasatinib. In! g; s. K: f, C7 a3 m7 l$ {
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
1 H4 u. [ O7 m9 e: o- S( h4 Zshow that the leukemic clone remains detectable, as we have previously shown in
& I1 E+ W% M. mimatinib-treated patients. Dasatinib-associated immunological phenomena, such as5 v) I9 U( ~6 J' h% H
the emergence of clonal T cell populations, were observed both in one patient
7 _. r5 T/ U0 _7 ?% d- Wwho relapsed and in one patient in remission. Our results suggest that the
! h/ Y; x8 e) Y% icharacteristics of complete molecular response on dasatinib treatment may be- g( Q! a3 G4 {. M5 x
similar to that achieved with imatinib, at least in patients with adverse
3 I7 J n) b7 K& ]/ Vdisease features.
% Y2 E! g( w( }4 i* g# x) z |