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。
: k: g5 Y& }1 s: W- 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。
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% G q6 M F% ^7 Y: S- J" u作者：来自澳大利亚' E1 t# @1 W) O: z6 v1 K. ?# `
来源：Haematologica. 2011.8.9.
, W# U: ]% O- B5 O/ G( qDear Group,2 ?: L3 Z4 k- A2 S0 k
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" m, a2 e" P5 j' w4 T$ g3 b
therapies. Here is a report from Australia on 3 patients who went off Sprycel) A- n9 R* L1 b; f8 m$ K
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
* k! z, j" I. x. {& kremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
+ H, ^' F3 k* X* hdoes spike up the immune system so I hope more reports come out on this issue.* V8 C7 \" Q+ c8 ]) L- L
4 I% X' k6 }. s4 A( Q H; P
The remarkable news about Sprycel cessation is that all 3 patients had failed
: ~1 u9 i+ g) A8 nGleevec and Sprycel was their second TKI so they had resistant disease. This is
4 w/ F( _9 R6 M1 G( g1 L ^! pdifferent from the stopping Gleevec trial in France which only targets patients
* i1 h b$ i5 R7 Iwho have done well on Gleevec.. c$ A8 k# i9 T% F; b
- ]0 Q4 Z3 Y& Y: b+ S9 j, EHopefully, the doctors will report on a larger study and long-term to see if the" r2 Q4 t4 G5 \
response off Sprycel is sustained.
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/ ?- w8 g; T8 c" s0 s. _Best Wishes,
; b7 a! R& ^+ X) `3 k0 I- OAnjana
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5 ^3 }2 w# c7 U+ {4 e
% l% P7 ]& H/ l ^0 RHaematologica. 2011 Aug 9. [Epub ahead of print]( F0 R( Y2 H1 Y
Durable complete molecular remission of chronic myeloid leukemia following% f0 `" {3 ?, E
dasatinib cessation, despite adverse disease features.
6 c: i& S4 R& G9 B0 O( x% A( y5 VRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.+ F8 o: L! t) J' M
Source
$ ^* p2 Y' I4 S7 {6 Q- K, ~Adelaide, Australia;+ \: n3 t$ N" f/ f0 a) }' e' Z
: i- ]! ]3 H0 r7 p: m, W' NAbstract
- ]! Q" o$ X* ^Patients with chronic myeloid leukemia, treated with imatinib, who have a1 @$ b. W* ^! G4 a; O: G% T- k
durable complete molecular response might remain in CMR after stopping
5 R' v3 V, D( s8 i1 ^treatment. Previous reports of patients stopping treatment in complete molecular- m! H$ P; d) g+ ]: Z
response have included only patients with a good response to imatinib. We
' M# p7 z6 q% S. M' w3 d- Adescribe three patients with stable complete molecular response on dasatinib, H+ s4 w1 S" `- T& x
treatment following imatinib failure. Two of the three patients remain in
' A+ D8 e2 l; n% @% vcomplete molecular response more than 12 months after stopping dasatinib. In
2 i: `6 y( I Rthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
+ Z: T" s& p. I2 Z$ j! c: ishow that the leukemic clone remains detectable, as we have previously shown in
: N8 s! R3 t1 g [1 ]* Zimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
7 K6 h9 E1 o( \) Q7 I3 J% b1 q' Lthe emergence of clonal T cell populations, were observed both in one patient( ~5 T1 U, B; k: I; M9 X
who relapsed and in one patient in remission. Our results suggest that the
. N: t0 \$ r0 d! o/ V$ m3 E Kcharacteristics of complete molecular response on dasatinib treatment may be
- ^4 w+ |0 I( @4 B5 u% Ysimilar to that achieved with imatinib, at least in patients with adverse
1 r G1 N( ?8 N" j; B9 ?disease features.
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