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。
0 H) n) K% e3 Q6 G7 G& 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。( X2 z+ |! U, s" d
) L1 o* ^, z ^/ i/ H9 J3 D作者:来自澳大利亚1 N F* }5 G6 q1 j J
来源:Haematologica. 2011.8.9.
* z) w* [# m* B8 ?& WDear Group,! G3 F7 W# }) R9 V& P7 R, w1 t
3 n" m! _7 A/ a6 J: U' ^! o6 s9 ?Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
! F. x4 v, q8 ]+ W% Btherapies. Here is a report from Australia on 3 patients who went off Sprycel- ~% d" X* }& m" |2 }; j7 n
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
s! L, J0 @2 q" F3 i# q, \ g7 @& }remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
* J. N4 ~) n9 t8 i! F# tdoes spike up the immune system so I hope more reports come out on this issue.
; t( M- J; E7 p! [
8 b( ^* F( I* t4 d: ]) T0 U& MThe remarkable news about Sprycel cessation is that all 3 patients had failed. a a0 g$ u* ^8 Y- q
Gleevec and Sprycel was their second TKI so they had resistant disease. This is P% Y+ b3 y6 A: q4 w+ S# k0 _! C
different from the stopping Gleevec trial in France which only targets patients4 \" {' T# ]& y3 \* \2 l( g& ?: b0 j) F
who have done well on Gleevec.0 A1 o3 m) L1 ~, g( U7 y) G$ d
# R( ]1 h% _% U, a% P: jHopefully, the doctors will report on a larger study and long-term to see if the
% f( q6 q0 s7 U( C/ I5 I& ]3 oresponse off Sprycel is sustained.& F5 [6 p; I/ d$ F( s, } D
0 F: o/ s* n iBest Wishes,
$ {% D% h- ]! s- Z$ X: v- v, `Anjana$ H" `9 u" J e( y0 ^) x! _8 u
: s$ f+ N, J7 W# r* _& {
- `" a$ ]1 B0 O, t) |7 Z; q
F G$ W0 e) a( n! d0 ~Haematologica. 2011 Aug 9. [Epub ahead of print]! t3 I2 X+ }4 g
Durable complete molecular remission of chronic myeloid leukemia following( G# {( w" B+ K$ G. g( z1 {6 Z% h
dasatinib cessation, despite adverse disease features.: X2 R3 D8 L" G) D( {
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
' @; ]* `# Y% x- Q) T5 q3 DSource
1 R* j8 ~$ P* aAdelaide, Australia;. P, y! Z9 E0 u- R ]6 I t
G, B, z! Z% u" C5 F) SAbstract
# F. w* B- y* [4 ^5 [! H. n5 NPatients with chronic myeloid leukemia, treated with imatinib, who have a8 x1 F5 V0 w6 a. K c
durable complete molecular response might remain in CMR after stopping
2 @ u _' T) Y. u( Z y8 x2 Streatment. Previous reports of patients stopping treatment in complete molecular
0 A h+ Q' _# \6 @5 hresponse have included only patients with a good response to imatinib. We
7 z6 Q7 v! T1 ? D N K# X* ddescribe three patients with stable complete molecular response on dasatinib7 |) }5 @: Z, w1 _. x r+ E
treatment following imatinib failure. Two of the three patients remain in6 e. v2 [1 r4 i- F
complete molecular response more than 12 months after stopping dasatinib. In
3 C$ i' s% L; {/ bthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to* b' c- {0 E/ D
show that the leukemic clone remains detectable, as we have previously shown in' r# n% h- t1 G
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 D% [# |* S& ?, g7 R: _1 Vthe emergence of clonal T cell populations, were observed both in one patient# E1 [& \' \8 R5 O1 ]/ b# _" b
who relapsed and in one patient in remission. Our results suggest that the
3 S/ A; Z9 z. q/ Ocharacteristics of complete molecular response on dasatinib treatment may be: H7 U3 q9 p" d1 G7 c; G6 E" M
similar to that achieved with imatinib, at least in patients with adverse
5 B, ^' C; j( h3 |" C4 Bdisease features.4 L, `( y6 T" i4 E# Q, @
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