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。# V3 z5 T/ l- ^) v4 A" ]
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。. J: Y+ v% I8 |; F: k# ? j
" H& D3 }7 ?1 L0 W& d( h- [作者:来自澳大利亚2 _5 W! O8 g. @' E2 Z/ M
来源:Haematologica. 2011.8.9.& c8 k( i6 B' P @# z+ M) i
Dear Group,8 B8 J6 x( _8 L
8 u) n) x7 B+ E6 F. V6 \. U& f) f) RSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML3 r- `; B, N0 I' D8 R
therapies. Here is a report from Australia on 3 patients who went off Sprycel6 a8 p4 p3 o: N: O
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients ?4 v' d0 |" J) d% l7 O$ v
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- j0 @% \) P+ N) U$ O2 Mdoes 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
y& Q2 o' D7 r" [5 ^/ t, ZGleevec and Sprycel was their second TKI so they had resistant disease. This is
# {. {% V9 t) e0 \6 O- A# Y- Kdifferent from the stopping Gleevec trial in France which only targets patients
# ^$ d5 A1 r- s! `2 H' ^ a: S0 Owho 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
. V$ t0 Q# y3 @2 F) Iresponse off Sprycel is sustained.2 ~# w$ p! W- `" Y2 t5 z
5 r9 X4 E. D/ D5 F( i+ W/ t
Best Wishes,
) v, h2 B/ W, SAnjana
4 m7 {$ T/ E3 v. r/ d Y; h" o3 I" n5 k5 @* G4 c
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3 D5 r$ V, Q. }! @Haematologica. 2011 Aug 9. [Epub ahead of print]
( l$ s8 I( p+ X( a- [Durable complete molecular remission of chronic myeloid leukemia following6 j N+ v3 ?8 j# h
dasatinib cessation, despite adverse disease features.
5 W# I: F# _& u4 X+ H+ u5 L/ yRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.- [" J# b; i( Y6 g( H e& f8 |% t
Source
- ]4 p( U$ p) YAdelaide, Australia;
# [( p" z& ~; J- p l5 w- z+ S( |) ?( _, h/ {
Abstract! d+ {! |" K" W7 ~4 z2 C9 k
Patients with chronic myeloid leukemia, treated with imatinib, who have a
2 d2 o, N# S! p6 E" h; `/ Xdurable complete molecular response might remain in CMR after stopping
) ?& i8 x" c$ }( |8 Rtreatment. Previous reports of patients stopping treatment in complete molecular
* o) h1 }$ Q* @+ lresponse have included only patients with a good response to imatinib. We8 z3 v4 w L4 p8 w# z
describe three patients with stable complete molecular response on dasatinib) B3 S2 ~2 z! A* t1 H6 O1 o
treatment following imatinib failure. Two of the three patients remain in
/ P- ?5 T: N5 e: q+ Tcomplete molecular response more than 12 months after stopping dasatinib. In
8 |/ y9 H" Z( Jthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to" @1 {$ x+ @! F( b1 k! M! B w a
show that the leukemic clone remains detectable, as we have previously shown in
3 G: m" D& K5 Y: T- mimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
, B2 m1 q9 F, ~the emergence of clonal T cell populations, were observed both in one patient7 Y6 X+ k' z5 }. D: c! V! C
who relapsed and in one patient in remission. Our results suggest that the
7 g& n& n0 |. a pcharacteristics of complete molecular response on dasatinib treatment may be
0 j; x6 ` }' T. m- }, ?similar to that achieved with imatinib, at least in patients with adverse
e* Q: ^0 F" ]8 `; S, Udisease features.
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