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。& T5 N8 J2 l/ w2 o
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。* ]" i1 A, f* ^/ G
$ l5 v& I) g2 h* X1 m5 \作者：来自澳大利亚: f% W" F) h5 B
来源：Haematologica. 2011.8.9.
# f/ \: M6 D, u; fDear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
0 W9 C1 ^( X, c( @7 b1 N: { q( {9 Rtherapies. Here is a report from Australia on 3 patients who went off Sprycel
0 y% D R8 f7 D! t! I1 vafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
1 } P9 ^8 [9 U8 K) Yremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
4 V3 a7 a. K& ^+ c" \, Adoes spike up the immune system so I hope more reports come out on this issue.4 r, p$ f& s* O8 S# a7 @7 @1 s
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The remarkable news about Sprycel cessation is that all 3 patients had failed/ e! g" x2 w8 T- X' C4 J) ~
Gleevec and Sprycel was their second TKI so they had resistant disease. This is% ~" e5 D) e. B0 K8 m1 M+ _- g% K4 O
different from the stopping Gleevec trial in France which only targets patients1 ?1 |1 r0 t& {
who have done well on Gleevec.7 V) T i8 P* `) g0 x/ n
6 d7 q; _$ a- Y. N/ d3 n1 SHopefully, the doctors will report on a larger study and long-term to see if the$ G! p) _$ W0 _7 T% r) a
response off Sprycel is sustained.
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( J) h' L" k( Q8 @' D& Z* |Best Wishes,
' M1 f7 A, x! b) H' s4 U E; ~& FAnjana
9 i# _7 z5 @: u8 r! a4 H
/ a& Q2 P% T1 y0 q- S7 o7 d7 n
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& z. {4 X* z6 o, F1 g* iHaematologica. 2011 Aug 9. [Epub ahead of print]
& D/ }4 L" D7 y, t3 e2 j$ TDurable complete molecular remission of chronic myeloid leukemia following
% C f5 z) R( W: I6 D* ^dasatinib cessation, despite adverse disease features.7 s# ^9 w+ B5 E
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 L) M0 I1 u- D' w4 m8 a
Source
5 K: A$ z! e: K$ a! x' L6 IAdelaide, Australia; `7 h0 W4 }; |3 h$ R/ q* g
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Abstract
) R% m1 e, @5 c2 q3 wPatients with chronic myeloid leukemia, treated with imatinib, who have a5 p1 i3 Z n% P) c
durable complete molecular response might remain in CMR after stopping0 Q3 F# Q$ s/ T; f
treatment. Previous reports of patients stopping treatment in complete molecular& x G1 A+ K0 i% Y% m! l
response have included only patients with a good response to imatinib. We
4 w6 j* U* {& e* I9 c" c1 d; Udescribe three patients with stable complete molecular response on dasatinib
6 u' v8 y- M/ X& t6 {( xtreatment following imatinib failure. Two of the three patients remain in
@ D: ?9 L; _% V, G& \complete molecular response more than 12 months after stopping dasatinib. In
' V* c$ j. y6 S: E! a2 h1 x5 M& Lthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
. j+ F, A- W$ U: A# Z7 m# ishow that the leukemic clone remains detectable, as we have previously shown in" R1 o8 `, x0 m$ u; @% s% {2 u
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
6 ^8 ?- P- B; q3 T$ ?, Dthe emergence of clonal T cell populations, were observed both in one patient
d W8 e a$ r3 H: `who relapsed and in one patient in remission. Our results suggest that the' \6 ?# g. K/ l5 \) n
characteristics of complete molecular response on dasatinib treatment may be) k6 J- ]4 x; I& W2 W
similar to that achieved with imatinib, at least in patients with adverse( I& t. q _. B& [' ]
disease features.
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