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 h) B0 Z+ |( @" 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。% r# v) ?! O1 ^' t1 ?- u, D
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作者：来自澳大利亚
& R# ?3 A- [ }来源：Haematologica. 2011.8.9.$ Q* W5 d7 f% e, U- x- e0 ~( m
Dear Group,% S6 G3 q" y1 t
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
4 \; m0 z4 ]9 k( M5 i/ J3 ctherapies. Here is a report from Australia on 3 patients who went off Sprycel$ R4 t7 d0 L& c/ u! o' u
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
t5 ]# W1 L: ?/ g8 u3 k Zremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
& ~. V2 Y b+ B+ m/ zdoes spike up the immune system so I hope more reports come out on this issue.9 q7 D9 b, p* G9 w
1 Q4 t2 C4 z( zThe remarkable news about Sprycel cessation is that all 3 patients had failed7 R& Y4 M. c! L6 `1 h
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 A' Y/ ~! z! Y" W
different from the stopping Gleevec trial in France which only targets patients* } @. m" @! M' T8 n! V
who have done well on Gleevec.
3 k% x3 @" b# \4 e! S
* t5 l ?/ W( B* h+ b7 JHopefully, the doctors will report on a larger study and long-term to see if the
6 Q! _1 I! i" K% Iresponse off Sprycel is sustained.1 I' P6 W, @, g' }3 O9 b* J6 {5 g
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Best Wishes,
/ I* Z* t K( @& z# NAnjana) Y6 ^$ E# f J; F! `+ J7 S
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& T, j; j5 H. S" g7 S9 N& b2 J% ZHaematologica. 2011 Aug 9. [Epub ahead of print]
% j0 c l- T/ NDurable complete molecular remission of chronic myeloid leukemia following
, B: g# j* R1 w! S# m, l' V( d" d) g" Vdasatinib cessation, despite adverse disease features.
9 E$ c1 p: h. N( NRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
) e9 ]8 H# e; K. q& s# G) CSource3 K9 a% I4 W% x6 H6 V8 P
Adelaide, Australia;
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5 ^+ b+ O- H, A; u1 f+ RAbstract* t) f: I; P% u) `% ?9 A
Patients with chronic myeloid leukemia, treated with imatinib, who have a# B! m: ^4 T I
durable complete molecular response might remain in CMR after stopping
; t9 H: Z. j5 T8 V; x7 {; k, p+ \5 d3 ztreatment. Previous reports of patients stopping treatment in complete molecular( ]% D# g' N. s2 R
response have included only patients with a good response to imatinib. We
2 O3 P* z% p+ e4 C" o5 qdescribe three patients with stable complete molecular response on dasatinib
, U3 J- J2 r6 _* rtreatment following imatinib failure. Two of the three patients remain in
z ^" \8 J( w8 C: K, q9 ]9 S! dcomplete molecular response more than 12 months after stopping dasatinib. In
" q) C1 o& Z0 L& J2 I" Kthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
% k! n0 a8 o+ ]) H7 ?$ w0 Kshow that the leukemic clone remains detectable, as we have previously shown in
( I" c! q- R J: C- S. oimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
4 {3 c/ n' I/ Wthe emergence of clonal T cell populations, were observed both in one patient3 g$ ?2 B) ~8 m
who relapsed and in one patient in remission. Our results suggest that the1 e6 T- w- M* `% s) G
characteristics of complete molecular response on dasatinib treatment may be; [# h4 \/ W+ b
similar to that achieved with imatinib, at least in patients with adverse& p$ G% H. G. j: p T% j9 P: ^
disease features.
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