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 j$ o* J4 }) C# w9 r! e
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。
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作者：来自澳大利亚5 M, E( u2 h7 D* V+ i( V( D6 k
来源：Haematologica. 2011.8.9.
; Z: z" k0 n( q$ f0 t+ C7 jDear Group,: y) s9 Z7 S, {. j( ]
8 N) `1 X3 ]+ O. Y- W: K
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
/ L2 \8 u/ A. g9 P0 ^' }. rtherapies. Here is a report from Australia on 3 patients who went off Sprycel
3 r) L7 C- U2 G2 Uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients; R* w2 o3 u2 E: ~& p2 D- |
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel4 d* w G! u( A
does spike up the immune system so I hope more reports come out on this issue.8 p( f" A" u* b- N, d
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The remarkable news about Sprycel cessation is that all 3 patients had failed0 d7 D* s3 ^6 [' p5 Y6 W0 {7 z9 j
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
, \, @0 Q/ P9 B. ^6 p, n& q$ pdifferent from the stopping Gleevec trial in France which only targets patients* {5 ^* i1 `; c7 K' ~; S: {! D
who have done well on Gleevec.* V* p2 o4 c# G4 H7 S9 z3 s7 W
1 k5 p5 o4 o8 k% ]# l! |& SHopefully, the doctors will report on a larger study and long-term to see if the1 _+ |. {. n- I" o! F9 L
response off Sprycel is sustained.
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Best Wishes,
9 a2 \9 L' O9 u n1 WAnjana3 X' ^4 b3 T$ u' |. _$ [
0 d" H7 ]! u' t$ ~2 r) }
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Haematologica. 2011 Aug 9. [Epub ahead of print]
, `- E% s0 @1 q$ g* pDurable complete molecular remission of chronic myeloid leukemia following
. r' w% s, E! x% s# G1 d2 A+ a+ J+ Ydasatinib cessation, despite adverse disease features.
1 z' v7 q5 u0 t7 A8 s9 b' `Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 Z: t" s' l' U3 X4 J) ^
Source
4 H7 Z6 r# v' a4 h+ ^. YAdelaide, Australia;8 [5 Q9 a( r; B& k+ C
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Abstract1 u+ a0 L/ f4 u ]4 Y! Q g
Patients with chronic myeloid leukemia, treated with imatinib, who have a& {1 q- \$ h x$ }& X
durable complete molecular response might remain in CMR after stopping3 i9 g2 C9 B. j6 V. c# j0 L) i
treatment. Previous reports of patients stopping treatment in complete molecular7 s5 F" G: ~: C7 u! c
response have included only patients with a good response to imatinib. We' M4 L1 m2 o4 f
describe three patients with stable complete molecular response on dasatinib2 J: V5 B+ d+ y1 Z! `
treatment following imatinib failure. Two of the three patients remain in
3 ~1 P6 E- p. Lcomplete molecular response more than 12 months after stopping dasatinib. In$ J7 y+ v0 p* H; k7 K
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
4 \6 `4 u) S& K! z: Y$ Tshow that the leukemic clone remains detectable, as we have previously shown in6 ~8 `% W! i2 T1 r
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as: D4 }7 l9 V1 x8 u5 H
the emergence of clonal T cell populations, were observed both in one patient4 O+ W; w8 q2 y2 s5 e4 m
who relapsed and in one patient in remission. Our results suggest that the* n, S- d1 x7 b1 }5 z' q6 t
characteristics of complete molecular response on dasatinib treatment may be# O" V/ C& q( t2 w
similar to that achieved with imatinib, at least in patients with adverse
& {( J' f# r1 T9 gdisease features.
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