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。' u, V- U/ {, I! c
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。
8 b$ D" m- q* s; ?/ M) n
1 J" }2 L* U+ H7 [7 @; t, o作者：来自澳大利亚: b, J: M3 [5 @! S& N6 H* x
来源：Haematologica. 2011.8.9.
4 `2 | R8 }8 p' \4 m0 yDear Group,
, Z% K0 B9 A) z6 a) L. W, ]( S
! [" Q2 S+ p3 ]0 f! ~Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML! j, E: L8 N3 I" G
therapies. Here is a report from Australia on 3 patients who went off Sprycel0 s6 t( t% V; z" X- h! K
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients R: O$ [; B* }7 e/ x
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
# G1 \' Y# ^/ d& C% ndoes spike up the immune system so I hope more reports come out on this issue.( Y& u) x3 P/ a! ]3 G- S P
. J1 V. N% I6 F# b
The remarkable news about Sprycel cessation is that all 3 patients had failed
8 X2 x: X. H4 a2 O+ Y# Q& RGleevec and Sprycel was their second TKI so they had resistant disease. This is7 ?* k+ [, d9 e
different from the stopping Gleevec trial in France which only targets patients
4 p Q" d {- s* j& o+ wwho have done well on Gleevec., `1 I/ @2 ?6 Q
* T* W$ z9 O: T* k0 U
Hopefully, the doctors will report on a larger study and long-term to see if the% a$ P4 b; v, l
response off Sprycel is sustained.: x! e% ^9 Q4 K0 R& K0 e$ n3 B
/ {& A: Z# O4 s" y aBest Wishes,
7 K& H/ }+ K# K! N, w2 CAnjana, N2 q, i) w9 x) ^: D( b
6 D. F" n1 d: G' y* d
/ V1 p8 S% ?: w5 n
1 T! s' y) f' O& U- q. x7 w5 ~Haematologica. 2011 Aug 9. [Epub ahead of print]
+ u2 d# X3 ~. g$ @$ s7 aDurable complete molecular remission of chronic myeloid leukemia following
& ?# }& z3 d0 l C# F G# Ndasatinib cessation, despite adverse disease features.& E% |2 E5 ^3 r/ H( l) G
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.0 |1 p, \" Y- D* R
Source- N" d: q G* A$ I0 l
Adelaide, Australia;
7 m O( z c- U/ H; b6 q. p
% O# N9 R( G7 i8 k$ ~+ ~& R& oAbstract9 W% N% R2 p. u* @1 U8 \. H
Patients with chronic myeloid leukemia, treated with imatinib, who have a% S& j6 L& k. F2 s. u/ n0 g( W
durable complete molecular response might remain in CMR after stopping9 r6 i* v* ]9 J/ m/ r, w
treatment. Previous reports of patients stopping treatment in complete molecular; ~7 o. D& T5 o" \0 b/ E
response have included only patients with a good response to imatinib. We! }; B* f' j8 C! v
describe three patients with stable complete molecular response on dasatinib
0 `- A% T) X* Y& X) v) d$ l" c$ otreatment following imatinib failure. Two of the three patients remain in
4 N0 D) F" i$ n* w6 U ~6 Wcomplete molecular response more than 12 months after stopping dasatinib. In; k4 T3 y. w; r* r1 `( {$ a H
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' M1 J+ E! u5 Jshow that the leukemic clone remains detectable, as we have previously shown in" K5 Z8 S( [2 _
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as5 c. K* J+ Y v, ?+ R
the emergence of clonal T cell populations, were observed both in one patient
8 s4 r6 H0 l& \4 N& k$ E0 gwho relapsed and in one patient in remission. Our results suggest that the
& P, r) e& C& F0 Q9 r& vcharacteristics of complete molecular response on dasatinib treatment may be
5 D- j/ H1 _7 T0 y; S0 g2 }% wsimilar to that achieved with imatinib, at least in patients with adverse
2 u6 W. m, V" b! k6 ndisease features./ Y" _" k1 z! ?+ d# f/ w, a
|
11011102001537 )
显身卡
