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。
' `2 m0 I9 w& Y 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 I) e# X0 g' h% n0 Y- l) K$ {- |
# i: L- @ H( q" O' O) Y作者:来自澳大利亚
# ~0 l* y F- S4 t$ U: Z7 B1 \& T来源:Haematologica. 2011.8.9.; j( J$ D7 V" z2 [0 I5 J9 W3 A; D
Dear Group,4 a* }& A }/ w# y+ m: V- X5 N" m
3 f4 U1 R6 K! X! p9 H
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
4 q+ q( b+ y5 P2 Y1 ]therapies. Here is a report from Australia on 3 patients who went off Sprycel* u. k5 M& Y9 Q9 k" V
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
7 ^& f( \1 E P+ S. L& iremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
* ~, O+ R) t$ Jdoes spike up the immune system so I hope more reports come out on this issue.
( I4 k( _9 {4 Y/ v O' Y2 n
0 U+ d& z' T6 t/ F3 ?, lThe remarkable news about Sprycel cessation is that all 3 patients had failed% n2 c6 Z3 W$ i( O4 s
Gleevec and Sprycel was their second TKI so they had resistant disease. This is: Q! [9 w- u. w3 X
different from the stopping Gleevec trial in France which only targets patients
( K0 F8 Z' g& m! ^5 D1 Lwho have done well on Gleevec.* T/ C4 E1 I$ t
) ?/ R6 R7 k) ~5 y+ u
Hopefully, the doctors will report on a larger study and long-term to see if the
/ ]/ T6 e h6 T) H' u1 s4 Vresponse off Sprycel is sustained. b, I4 J; t7 |# X: B8 G# \1 y
" N5 l1 s) l3 P% T6 T% `% E3 RBest Wishes,
, V+ x3 w+ \* k$ fAnjana
! L+ M# T$ p/ R# ?4 `# m% T8 D/ p2 h3 Z
, Y8 W( u4 n: p
) u: q# ]3 ?6 J; k$ {' d. AHaematologica. 2011 Aug 9. [Epub ahead of print]
& t( T6 H' J. E; i: S/ b& x% S) wDurable complete molecular remission of chronic myeloid leukemia following
2 |" ]7 O- r/ Y- Q; @8 Z7 k# edasatinib cessation, despite adverse disease features.
6 W2 P* r6 W' Y* @3 ERoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.& ]3 e4 k+ M/ r$ {# L& k, {& U! d" j
Source. {5 e9 P: i! X. s% e E% q0 E
Adelaide, Australia;
# b0 g- q8 D9 |# ^ y
1 @) f- D9 a C7 G' s& @Abstract" t) F& Z+ U5 O! P
Patients with chronic myeloid leukemia, treated with imatinib, who have a
9 S! n7 E" Q: _+ L% e& Z- [durable complete molecular response might remain in CMR after stopping
9 n9 |5 d. t2 O' T7 Ltreatment. Previous reports of patients stopping treatment in complete molecular
) O# E9 U" b; ~8 ?- N! I) I4 `response have included only patients with a good response to imatinib. We
' [- v4 ?- }" k8 ^2 Bdescribe three patients with stable complete molecular response on dasatinib
4 N# i/ }& o- h4 ytreatment following imatinib failure. Two of the three patients remain in) B. s! U4 F$ u: n4 f
complete molecular response more than 12 months after stopping dasatinib. In$ X+ h" I* Z# X3 z
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
% O% M: W( [" |( ^$ pshow that the leukemic clone remains detectable, as we have previously shown in2 a0 ?4 S3 P/ y$ T4 f6 i( F
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as) O2 ^6 ~, D' F
the emergence of clonal T cell populations, were observed both in one patient
& Q) Q% s: ~ z5 v1 qwho relapsed and in one patient in remission. Our results suggest that the
3 S. M" p5 E# ^; A* ocharacteristics of complete molecular response on dasatinib treatment may be: j, A, L( Q9 j: s. }8 ?
similar to that achieved with imatinib, at least in patients with adverse
* k' W0 t& g4 Wdisease features.& c% f; `) }$ J: R/ L- _$ o, V
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