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。( l; q% F, i% k: Q* r9 y$ F
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
, i# F$ s0 P6 F5 c/ W来源:Haematologica. 2011.8.9.( ?; ^& w. D$ v1 w5 F" Z
Dear Group," b7 ^6 e* G# J
g. Z; C4 Q; I8 oSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML/ l/ S" @5 Q: q
therapies. Here is a report from Australia on 3 patients who went off Sprycel
7 [6 ^7 o6 \2 C2 H* {1 Mafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients' V/ b5 S( v+ b$ }7 u4 U
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- R# f+ @/ w( p3 l" T0 Z( ndoes spike up the immune system so I hope more reports come out on this issue.# P; `0 l6 Y0 u# A" X* E
1 t/ ]8 O9 ~* Y6 J( UThe remarkable news about Sprycel cessation is that all 3 patients had failed
7 Z k! G+ x8 ] }3 `Gleevec and Sprycel was their second TKI so they had resistant disease. This is
# {; D$ q' {/ o1 Kdifferent from the stopping Gleevec trial in France which only targets patients
# n6 y/ |0 B! m; j- a3 Pwho have done well on Gleevec.$ }. H# L7 _( M8 [3 z
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Hopefully, the doctors will report on a larger study and long-term to see if the! ~$ s' l, L8 V; U+ q6 T
response off Sprycel is sustained.! G7 w" l* T4 X' Y
+ j' V) M4 c( YBest Wishes,
3 |: d! o" K4 m2 E2 ]5 F9 eAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]% s0 k% T( L. W* J0 ^6 K# U
Durable complete molecular remission of chronic myeloid leukemia following
' { w% b7 a- y$ i: z' p. H& ddasatinib cessation, despite adverse disease features.
, S4 {, T' `. @" T8 g% oRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.- J8 {4 o* n3 Z) S, [4 h% f8 r ?$ O
Source& w5 b: Z/ \8 y
Adelaide, Australia;6 @1 z7 e( u3 x$ `
8 P) a# Q' d8 O; F% i8 |Abstract% z# u1 `1 @$ @
Patients with chronic myeloid leukemia, treated with imatinib, who have a. i2 E7 ?" `" O; c* Y" H0 N
durable complete molecular response might remain in CMR after stopping
& w& r/ u3 T z: H% U+ g: c+ mtreatment. Previous reports of patients stopping treatment in complete molecular' L% v; C- u* e% J8 P5 E
response have included only patients with a good response to imatinib. We
# k4 p: u! {0 O/ B* D, L6 udescribe three patients with stable complete molecular response on dasatinib
" w" v3 H3 B/ ~% R; Dtreatment following imatinib failure. Two of the three patients remain in w* I& [" o; C# U" k) m: b
complete molecular response more than 12 months after stopping dasatinib. In- k* L# |3 a2 J& o
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* H e0 ?2 A# \$ C" |' `) Vshow that the leukemic clone remains detectable, as we have previously shown in, Z& ?8 d% k- j
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as, ~3 N# D( P- N9 ~5 ]
the emergence of clonal T cell populations, were observed both in one patient' |- J& K+ T+ y+ i8 a
who relapsed and in one patient in remission. Our results suggest that the
5 J% o8 }5 B7 |6 ^- }characteristics of complete molecular response on dasatinib treatment may be3 Z9 N) ]1 v2 ]- Y' X# L
similar to that achieved with imatinib, at least in patients with adverse2 K0 ]) M7 K' U( I0 ?
disease features.
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