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。- { _% F ^) E# V$ k
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。. \' j: D B! |/ z! c: p- V
, N* q$ |* D; V2 S& w' C3 @作者：来自澳大利亚. _4 z9 k# d3 p& _
来源：Haematologica. 2011.8.9.
: D6 q6 i+ l& M; g; YDear Group,% \( a$ @( }3 t q: J6 O# [! d8 @
9 I) }; ?: \- J% ?9 B$ N
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
6 b. @6 n/ J2 Utherapies. Here is a report from Australia on 3 patients who went off Sprycel
4 V5 M* v. f$ F0 Dafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
7 n8 t9 y: W/ [4 p! s( xremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
6 t0 e/ w9 w/ M Zdoes spike up the immune system so I hope more reports come out on this issue.& V+ z2 E! D' R6 j" s' e
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The remarkable news about Sprycel cessation is that all 3 patients had failed
/ r& e* ]0 c8 OGleevec and Sprycel was their second TKI so they had resistant disease. This is
6 D g$ @6 s) n# \. |different from the stopping Gleevec trial in France which only targets patients
4 o5 t& b- }5 a1 i/ bwho have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the; U7 O6 ]3 g# k S6 e8 Y/ l
response off Sprycel is sustained.7 N: a* ~- z- |: ]. w
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Best Wishes,
8 t+ R& \1 ?4 gAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]
9 m( t2 L9 J* q, f0 H* l* o7 UDurable complete molecular remission of chronic myeloid leukemia following4 l0 m+ h( s$ P9 }3 K4 C$ ]
dasatinib cessation, despite adverse disease features.8 m" G0 N* Z" D9 |$ F$ d1 m
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.' ^7 z3 n- V2 O% G, a0 k- H
Source7 Z: u# r) j' f/ K; c$ h6 g) F/ @
Adelaide, Australia;( X2 H( v+ \8 J0 l
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Patients with chronic myeloid leukemia, treated with imatinib, who have a8 Y- y( `) a% {6 f2 _ H5 Z. k- S1 b
durable complete molecular response might remain in CMR after stopping' \. [' @+ [ k# J. t' q" Q! j
treatment. Previous reports of patients stopping treatment in complete molecular
) G% H0 V0 u: b1 Rresponse have included only patients with a good response to imatinib. We
- f* p2 `1 a0 Q1 Ndescribe three patients with stable complete molecular response on dasatinib
& ?: x! Z+ a) s2 }$ s8 W! A% otreatment following imatinib failure. Two of the three patients remain in; @ D8 ?6 k, \$ V; s
complete molecular response more than 12 months after stopping dasatinib. In
v& ]/ }1 ^+ jthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 M- e7 @7 x" R5 _
show that the leukemic clone remains detectable, as we have previously shown in3 N { I6 M8 S+ X; P$ z: d
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
7 I# s# |+ ~) U3 |the emergence of clonal T cell populations, were observed both in one patient
3 L( t" M% z2 @+ ~who relapsed and in one patient in remission. Our results suggest that the
' l! K' E9 v+ s' i% ?2 b7 L' mcharacteristics of complete molecular response on dasatinib treatment may be6 j3 @5 y% P- b+ Q6 a% d
similar to that achieved with imatinib, at least in patients with adverse+ o Q3 a1 T M% D
disease features.
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