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。
( J2 G1 U2 j" n6 R 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。' v4 o' S, `& y" e6 h& B
$ I% L: S! }5 c: n( Q作者:来自澳大利亚4 u) T3 V, K( t L D- C7 V
来源:Haematologica. 2011.8.9.$ H m) y# j( y8 U$ m7 A
Dear Group,
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! q& V0 ?% r/ u6 S7 c7 s- oSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 _% a3 P: f0 ]) P. e w4 I
therapies. Here is a report from Australia on 3 patients who went off Sprycel
' i7 G! t" M* j ~' S, Safter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients6 W0 f1 V% u2 V- e+ p: u
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 d) N. C9 u0 H1 A" R( e
does spike up the immune system so I hope more reports come out on this issue.
2 b1 y% j& M4 E: M, G7 F& v' Z6 S5 g$ R3 l3 r; f
The remarkable news about Sprycel cessation is that all 3 patients had failed
# r) ~5 K" I) h' `. X- l7 SGleevec and Sprycel was their second TKI so they had resistant disease. This is
' B; H1 ]4 T6 U- H- m: {1 v/ K. vdifferent from the stopping Gleevec trial in France which only targets patients
) Z0 N/ T. l. G) }0 ?6 a3 Wwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the: y. J2 N5 {% a. Z3 J
response off Sprycel is sustained.; p, a, V2 n0 D) u8 O
( Q" a0 J$ a6 bBest Wishes,3 d3 \& Z: J6 f* ? [
Anjana
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6 o2 E+ T2 d/ F2 ]
- d$ k0 s4 y# S8 g& rHaematologica. 2011 Aug 9. [Epub ahead of print]2 M8 k! m+ V5 e* ~1 B: t2 n8 j
Durable complete molecular remission of chronic myeloid leukemia following
0 S' v3 J. T1 E1 H, y. x( {dasatinib cessation, despite adverse disease features.0 b) h6 q+ Z: g* r
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
) r- @! K3 C4 g z( XSource
# d7 B. C) Z, p$ o! s2 f' l% e, eAdelaide, Australia;! Y6 {/ j# i; O, e! a5 S
! j! f; j% Q3 x: JAbstract' W3 {2 j1 c# h H4 ^/ w$ r/ @" q+ Y
Patients with chronic myeloid leukemia, treated with imatinib, who have a' I& v) A- Z6 ?, W9 R
durable complete molecular response might remain in CMR after stopping
" d2 f' S9 R$ }1 I+ V0 N1 gtreatment. Previous reports of patients stopping treatment in complete molecular
( w& y% x8 d) p- e& { i3 ?% Qresponse have included only patients with a good response to imatinib. We( r3 n7 G# Z; }- X7 J+ _# I4 J0 e
describe three patients with stable complete molecular response on dasatinib
- E- a* f3 r( {treatment following imatinib failure. Two of the three patients remain in! K* U; l. R' t0 m. R7 s5 I3 K% Y" B0 U
complete molecular response more than 12 months after stopping dasatinib. In
+ g# w4 {6 m/ s# e7 jthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
5 j. q+ j2 ?& bshow that the leukemic clone remains detectable, as we have previously shown in
1 W& Y: S9 r9 V! P5 yimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
& H8 c0 F. P P) e/ Ythe emergence of clonal T cell populations, were observed both in one patient
" t7 X7 ^' r' D+ ^0 ewho relapsed and in one patient in remission. Our results suggest that the
$ V& v3 b3 S- y& N! x/ ccharacteristics of complete molecular response on dasatinib treatment may be& m& D( X. u. a N% v( S7 n
similar to that achieved with imatinib, at least in patients with adverse$ F- C. _* p. y) _4 c4 p
disease features.- ]" i- `# `) E) G+ b8 A4 k
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