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。! ^$ w, |" w' P7 S& w7 j0 Q
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。4 J% {( X9 K6 w. H8 v
$ o- E+ u% x y作者：来自澳大利亚
: h4 O5 N/ M9 o* D6 m( c来源：Haematologica. 2011.8.9.
5 } o% H9 b; p$ z/ g5 JDear Group,! o& k5 {9 ~' R& }) h. ~4 Y8 |
) ?9 {! M% r6 Q( h o- P
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ T5 v" O0 n3 K y
therapies. Here is a report from Australia on 3 patients who went off Sprycel
$ E8 i# P% w9 z; Nafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients$ r( a4 z; ^2 g
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
% m! p/ N3 f% v/ f+ bdoes spike up the immune system so I hope more reports come out on this issue.
" {9 f' [. I" a2 Z) V' I2 Y; R9 L1 i/ ?; [6 R; Q
The remarkable news about Sprycel cessation is that all 3 patients had failed
+ B7 {4 I; J3 E/ }/ M+ d hGleevec and Sprycel was their second TKI so they had resistant disease. This is% L! d7 |$ j2 q8 e
different from the stopping Gleevec trial in France which only targets patients9 ^! J k p7 v$ Z* W: ~, ^9 F
who have done well on Gleevec.
. g5 b) a. S5 \0 ]- L: z
4 \% r/ ?. ?! g" \6 d; h4 zHopefully, the doctors will report on a larger study and long-term to see if the8 g- q$ i/ x: S( k0 ^3 T9 J
response off Sprycel is sustained.
8 i/ H, h1 s( f5 q7 J! q" s! P/ N
Best Wishes,8 g- S& n( j# n3 r) [! t: q# K
Anjana5 N# M4 h) C8 q: I& l+ O
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3 `; y9 q$ P+ ^9 K0 A1 n
Haematologica. 2011 Aug 9. [Epub ahead of print]$ E, Z0 G6 q* J$ L* W4 D
Durable complete molecular remission of chronic myeloid leukemia following5 B! T# d+ n" E, j$ a' x
dasatinib cessation, despite adverse disease features.
% \8 z9 d( w8 Y1 ~0 ZRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.; n( g/ f0 [ k- T
Source- N8 q9 |, A% f( Q9 v
Adelaide, Australia;
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Abstract
& `4 ?: S8 T) G6 R sPatients with chronic myeloid leukemia, treated with imatinib, who have a
, y: s p1 n0 n8 Z* tdurable complete molecular response might remain in CMR after stopping" H7 Y/ m1 i X+ l0 }
treatment. Previous reports of patients stopping treatment in complete molecular
/ F! @2 x: E" o, yresponse have included only patients with a good response to imatinib. We
9 S9 J* z0 m/ T; F5 Tdescribe three patients with stable complete molecular response on dasatinib
1 j2 H4 X& }, ^8 j- a+ D; Streatment following imatinib failure. Two of the three patients remain in
8 H0 z1 n2 I% @) M. i' bcomplete molecular response more than 12 months after stopping dasatinib. In' U. l g+ v7 a$ f" b7 J7 o
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
+ _9 F; i2 U7 g( J* @' p$ T, a' V! Eshow that the leukemic clone remains detectable, as we have previously shown in/ |$ U! E$ n/ v3 i& K
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
1 p5 X5 b3 c0 m4 J! Ethe emergence of clonal T cell populations, were observed both in one patient4 Z8 Z; Y7 d" S+ @, t! D! @
who relapsed and in one patient in remission. Our results suggest that the
$ o! ]# n/ I c L# |characteristics of complete molecular response on dasatinib treatment may be4 L$ t4 d0 h) w+ E T
similar to that achieved with imatinib, at least in patients with adverse4 i1 {. X; y2 _
disease features.! L/ b1 Q1 J& L M+ }
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