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。5 S" v8 `3 ?3 e+ l
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。 \5 f% t/ G. F6 G
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作者：来自澳大利亚( Z) v* M/ N! y
来源：Haematologica. 2011.8.9.
3 e# [# [3 m0 fDear Group,) ]* F- A3 i* @" `$ W2 r7 q- `4 g+ j( S
, a1 W8 J" S" G) @9 tSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
h7 I$ v8 q, E% Y6 _) i; D/ E- P0 Stherapies. Here is a report from Australia on 3 patients who went off Sprycel
( t# q, U9 b4 D, k/ v4 m tafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients5 v: { i6 b* j7 R! H) u
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
! w0 e. B( I: @0 }/ sdoes spike up the immune system so I hope more reports come out on this issue.: {' W" L6 d! O8 u
! j! I4 F$ A2 e% Z/ x! F0 C* dThe remarkable news about Sprycel cessation is that all 3 patients had failed
" I; N1 v+ l+ t7 b6 RGleevec and Sprycel was their second TKI so they had resistant disease. This is
w1 Z x4 P6 I; b0 ]different from the stopping Gleevec trial in France which only targets patients% @; e1 P0 g% f7 W
who have done well on Gleevec.
7 j. P" X' V, a9 P; @' }" _' v
% r: ]8 j7 f4 H3 e1 wHopefully, the doctors will report on a larger study and long-term to see if the% Z. q( W2 H" S2 {( X
response off Sprycel is sustained.( h4 `! j- e5 p
. ? S9 t6 z' v j3 GBest Wishes,
$ {% E6 \ V# D) j$ gAnjana
% f; `6 _' b. m7 d. |' _
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Haematologica. 2011 Aug 9. [Epub ahead of print]
2 J3 T- F0 l# G; T6 f/ L" {$ L( cDurable complete molecular remission of chronic myeloid leukemia following$ E& s }& E5 Q$ E3 B1 Y
dasatinib cessation, despite adverse disease features.
0 g; ?2 A1 c1 r6 {0 I1 `Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP." ]# p4 R' P; R' S7 _
Source
' n3 K& k0 t% G, nAdelaide, Australia;
2 r& U1 B7 S0 p. f, {( X
|# n+ R; o- ^. dAbstract5 D- w/ u5 Q9 x. w7 C1 }
Patients with chronic myeloid leukemia, treated with imatinib, who have a
9 {2 r$ S9 s* y8 _9 W7 cdurable complete molecular response might remain in CMR after stopping
4 p. o7 e e# Z; `+ S& ctreatment. Previous reports of patients stopping treatment in complete molecular+ g. g3 Q. w" H* c- ]
response have included only patients with a good response to imatinib. We2 @- q1 l' q( X5 r
describe three patients with stable complete molecular response on dasatinib
: A; q# U, S5 u9 y) |treatment following imatinib failure. Two of the three patients remain in
( l' _. j3 k+ _complete molecular response more than 12 months after stopping dasatinib. In
9 C1 x" Y6 a+ @ w" j. j% ~these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to6 k$ D: u% z9 d, k
show that the leukemic clone remains detectable, as we have previously shown in" J X& F( K E/ p3 Y! b
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as- a2 b/ Q7 Q, N( l. k. b7 A0 d4 m. m
the emergence of clonal T cell populations, were observed both in one patient9 [' ?4 T& K6 y. i. x
who relapsed and in one patient in remission. Our results suggest that the' F: G! Y& _& u6 q G. B' K, h
characteristics of complete molecular response on dasatinib treatment may be
: b$ { \( i5 w& A: N4 _similar to that achieved with imatinib, at least in patients with adverse
3 Q+ h# H; K9 N( |disease features.
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