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。0 a8 T0 A. c& V7 _' K7 P
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。. D( j( Q! i& W' w, P
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作者:来自澳大利亚7 d4 `& e% \# ` A/ M
来源:Haematologica. 2011.8.9.
2 s0 q# b8 x& @/ y- ]7 }- Y6 k; `Dear Group,8 k+ F1 ~* U- G: O3 |% ]* t
1 \. q2 [2 [# XSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
: \/ |% k% C* @% \therapies. Here is a report from Australia on 3 patients who went off Sprycel
; k2 |0 H" u& @0 y3 oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
3 h6 T' y6 G6 K5 Iremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
: C# ?8 X% r2 W1 t8 g, F/ u0 \3 n. mdoes spike up the immune system so I hope more reports come out on this issue.& f/ X. e ?" T& @$ y1 h
9 c; d/ A. p% }# e7 v) pThe remarkable news about Sprycel cessation is that all 3 patients had failed
1 n& Q+ \4 B: b2 x7 F$ oGleevec and Sprycel was their second TKI so they had resistant disease. This is5 d+ R( U/ D& C+ o' R
different from the stopping Gleevec trial in France which only targets patients
+ K: ?# i0 s: d L5 V5 g/ `who have done well on Gleevec.
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( j* }. v3 \* ^1 PHopefully, the doctors will report on a larger study and long-term to see if the
) g! [+ F6 _2 D, ?0 rresponse off Sprycel is sustained.# [5 a7 O! ~% B" I1 K# u
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Best Wishes,: V9 j8 Y" h! l* @
Anjana
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' ^, d% O5 R- x0 }Haematologica. 2011 Aug 9. [Epub ahead of print]
& s' A+ _( t7 ^% cDurable complete molecular remission of chronic myeloid leukemia following5 K0 i& c3 w6 \2 L" o+ d( R
dasatinib cessation, despite adverse disease features.
8 y' }2 B, Z' V1 [5 rRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.* c, C5 R; t3 u. q# i% `: C
Source
# l+ w( P* m4 s$ n9 mAdelaide, Australia;
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Abstract U6 m/ c* f6 X$ ?
Patients with chronic myeloid leukemia, treated with imatinib, who have a
5 ~0 J+ `% W. ~( ]4 c- Ydurable complete molecular response might remain in CMR after stopping# X$ |( I% j% K% N E# E
treatment. Previous reports of patients stopping treatment in complete molecular- Q: w4 A" D0 N1 U
response have included only patients with a good response to imatinib. We$ ]1 J- e: p. B, _9 m$ X
describe three patients with stable complete molecular response on dasatinib
v: j# P- ?3 g8 M! j0 ]treatment following imatinib failure. Two of the three patients remain in6 |& T6 l6 V) z4 L$ h" P7 I" \
complete molecular response more than 12 months after stopping dasatinib. In4 x( s, I5 j6 e1 e
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to: j4 B3 f e! O" p6 V5 Z$ v; `2 t
show that the leukemic clone remains detectable, as we have previously shown in
% |" X$ L& @4 O, E& x# D2 u& ]imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
# ?3 l. R' {- H9 W3 v* lthe emergence of clonal T cell populations, were observed both in one patient
4 E& k, b% R8 O; O* \- Xwho relapsed and in one patient in remission. Our results suggest that the- N& u n% s1 g) {
characteristics of complete molecular response on dasatinib treatment may be
5 w8 a; U* _ ]/ U3 \similar to that achieved with imatinib, at least in patients with adverse
0 X& {( F" P2 d$ D% Qdisease features.- O! r* g' |# R8 W, Z5 u0 ]: v
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