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 D' y8 \* R: i% g! 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! V, C4 [0 j1 l- X V
9 K, t i3 Q ?
作者:来自澳大利亚" P( f( [% L! k5 C. g
来源:Haematologica. 2011.8.9.# e- n2 `2 t0 S7 H6 q8 X
Dear Group,
/ s. e$ n q, ^9 u. j8 A2 b( |
# p2 W; m; w/ c( c0 YSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML* h0 }( t2 T6 ]* v( R
therapies. Here is a report from Australia on 3 patients who went off Sprycel
D/ w8 _9 z" m7 Iafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients% m) U( b% g* t% Q7 w# _; `
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel$ J4 U% ?$ }" Q/ w# E
does spike up the immune system so I hope more reports come out on this issue.
' x0 ]6 w- d( o6 @( S
% a9 u' j: B2 ^The remarkable news about Sprycel cessation is that all 3 patients had failed
3 Z3 v6 {1 C$ B) ~Gleevec and Sprycel was their second TKI so they had resistant disease. This is
0 W6 M' { `+ R2 { L8 odifferent from the stopping Gleevec trial in France which only targets patients
* @; \* r; J: x! r0 K/ V' qwho have done well on Gleevec.0 m" w7 \1 a0 R: h% K2 z( w
3 C6 r" M. V$ L0 h# c
Hopefully, the doctors will report on a larger study and long-term to see if the5 Q3 E& Z3 X! @# D+ t z
response off Sprycel is sustained.
% P& f# k( O3 E
2 X Z4 b- ^" ^/ WBest Wishes,; u$ y1 C9 W9 O. \- o0 S J
Anjana( K+ P8 t0 H) [7 C
! n5 y* Y* u, t. D5 }
& q) H: y. |# u" p6 H) [& |/ @( u6 d2 X. I2 h: v9 D! ^
Haematologica. 2011 Aug 9. [Epub ahead of print]8 o, ^1 v; |) `/ U+ J! t% p) q
Durable complete molecular remission of chronic myeloid leukemia following
# l3 {0 U5 I+ p- }; z4 {dasatinib cessation, despite adverse disease features.5 K; D/ P9 r! t8 p; [; D
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.2 D7 K% k. G+ p# _
Source. R! u& |8 P5 d6 a7 m6 P6 t9 y( h
Adelaide, Australia;$ C, M X* I4 O/ |8 J# e3 v6 g
: m/ ~- b2 C( B5 ~; }: cAbstract- Q# d' c& m5 Q# z7 z) S" f" D& ^
Patients with chronic myeloid leukemia, treated with imatinib, who have a
% G; W5 X1 R9 J. n# ]durable complete molecular response might remain in CMR after stopping( i: n; ~- m+ v3 ~2 g3 k' g
treatment. Previous reports of patients stopping treatment in complete molecular
% m: L+ B* }3 ?3 f" y2 Y- V+ uresponse have included only patients with a good response to imatinib. We
9 Y) w9 d0 Z+ wdescribe three patients with stable complete molecular response on dasatinib, m: Q2 |3 f v6 N/ I
treatment following imatinib failure. Two of the three patients remain in' Q3 w8 v. d+ _$ s6 |
complete molecular response more than 12 months after stopping dasatinib. In+ H) y: `6 X) d$ W6 g+ r
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
# e. K6 o( w" F9 K8 bshow that the leukemic clone remains detectable, as we have previously shown in' R! G3 X1 U, @9 o
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as$ f6 R7 }6 I2 \
the emergence of clonal T cell populations, were observed both in one patient
: U" Z& ]/ S% H1 @: l! Mwho relapsed and in one patient in remission. Our results suggest that the# L; o- X5 I9 d+ Z" h
characteristics of complete molecular response on dasatinib treatment may be
+ S% n9 }3 I. [1 U( I( Wsimilar to that achieved with imatinib, at least in patients with adverse! \& c) M0 Z) v/ B* n- a
disease features./ d, I% ~4 ?/ T" p& E4 x
|