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。
4 P' y3 q! _4 ? 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8 c6 b- W# i2 M, a; h4 L
来源：Haematologica. 2011.8.9.4 K9 i% q" w# o1 A% z4 P
Dear Group," q- E- O. r3 ?+ p, l' z
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML" U, U) \0 G" {/ l
therapies. Here is a report from Australia on 3 patients who went off Sprycel3 Z& }+ Y- }7 Q0 l* L
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients8 I+ l1 y1 i" o( E' d' a: X; w0 C' K
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel0 f3 Y1 V* ^, W( ?$ t) f7 H8 A* ~
does spike up the immune system so I hope more reports come out on this issue.
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The remarkable news about Sprycel cessation is that all 3 patients had failed+ {6 f& A' ]) U$ c0 {! w
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
% T1 i$ o6 H5 N# Z8 Pdifferent from the stopping Gleevec trial in France which only targets patients
' o! F. C) `" |+ uwho 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% V7 |$ _3 f1 z
response off Sprycel is sustained.
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) I2 c1 q# t3 G# k) zBest Wishes,7 g6 @, g/ ~% ]* g) F! e9 V
Anjana* o$ A: S9 u' q7 V. t" t( b
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( e- V9 o# r4 C- n( ^Haematologica. 2011 Aug 9. [Epub ahead of print] O% B/ \$ v; h8 H- I& M. k% P: |
Durable complete molecular remission of chronic myeloid leukemia following
( X" U' |! [$ s+ q0 l8 |dasatinib cessation, despite adverse disease features.4 g! J7 E& U2 n; {0 _. H
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
5 R& C) v7 j2 q3 k) LSource' y& c9 j: P8 C$ v
Adelaide, Australia;
8 }) ^' X9 h; y, Q/ o% _/ l2 {5 q. u7 H0 L, I2 v! M( v
Abstract, J: @, }% J+ T3 y2 O* \
Patients with chronic myeloid leukemia, treated with imatinib, who have a
* ?: e& b) _, g0 c3 ?+ idurable complete molecular response might remain in CMR after stopping) \' h+ V( p5 D5 z8 Y
treatment. Previous reports of patients stopping treatment in complete molecular! A! x7 n& j4 j3 B- Q
response have included only patients with a good response to imatinib. We
7 ~& n! e* ~; r# S) y$ K1 J/ Qdescribe three patients with stable complete molecular response on dasatinib8 G+ _ T+ d6 a+ _/ a
treatment following imatinib failure. Two of the three patients remain in
7 g" [4 u7 S/ B) d9 Y. f( q Kcomplete molecular response more than 12 months after stopping dasatinib. In
) E* a* e9 D0 a. G3 v/ p8 e3 mthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
8 n: }+ X( G$ ~- M% Y3 g( oshow that the leukemic clone remains detectable, as we have previously shown in
- I/ T1 E4 Z4 P s" }imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
f7 d! H) R; r2 Mthe emergence of clonal T cell populations, were observed both in one patient/ {; @$ ~/ Z, \5 x. n: {
who relapsed and in one patient in remission. Our results suggest that the
, z. w: }" R5 B5 N( g/ S( U- z2 \( ?characteristics of complete molecular response on dasatinib treatment may be
: U" z7 N$ @4 y5 N- G% U: N7 Gsimilar to that achieved with imatinib, at least in patients with adverse" t( M; C R, m8 b/ m) ^
disease features.
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