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。
" j% A6 P, @/ @ 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。/ ?' f8 L' w1 H) ^# [' o- \0 M1 Y' }$ ~ y
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作者:来自澳大利亚0 h- E* [4 M/ x4 z$ v
来源:Haematologica. 2011.8.9.
# Q1 l( B/ t7 N. q3 t7 n# ]7 yDear Group,+ @' r8 n2 ~7 n) g6 h+ b
: N1 i0 J- B4 v& H) _ m2 `4 X+ LSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML2 i% B( c* H B0 m m" X
therapies. Here is a report from Australia on 3 patients who went off Sprycel
; A) }8 M( C. O& \% a U. X: Rafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
) n* O( T. z/ l/ S6 tremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
+ k- x! ~" p" C5 T7 d9 F+ Cdoes spike up the immune system so I hope more reports come out on this issue.; I# \- s, f+ y. Q8 p
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The remarkable news about Sprycel cessation is that all 3 patients had failed# [6 O) I$ ~+ @' x% U
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
u8 x& g/ v$ c6 O" l6 Kdifferent from the stopping Gleevec trial in France which only targets patients0 }- b9 \9 I1 r |$ f/ N, v
who have done well on Gleevec.2 q8 K- d: | e7 T0 y) N
4 E; w) E, f& h" D a1 RHopefully, the doctors will report on a larger study and long-term to see if the
/ P3 e, v3 z4 Jresponse off Sprycel is sustained.
# _- P, n9 w3 v, c" t# B6 G$ _2 V+ a
Best Wishes,1 z4 l4 k k) D& L
Anjana' @4 W) e6 X, C, m. Q' Y
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" {% U: Z# m3 E' `% m7 SHaematologica. 2011 Aug 9. [Epub ahead of print]! p4 s0 e7 e4 [
Durable complete molecular remission of chronic myeloid leukemia following9 I" j2 e- p9 B4 W
dasatinib cessation, despite adverse disease features.1 @4 m2 {5 U5 g' q' N( m
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
! ?8 ]- p1 G6 I ~: P* H5 S0 Q; pSource
! Q) G+ S6 ?- y$ K3 B8 I$ bAdelaide, Australia;
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1 T" N; s* O* [4 \( I0 bAbstract
6 G3 e4 U6 t5 f( o$ GPatients with chronic myeloid leukemia, treated with imatinib, who have a3 n1 \' a6 S' z4 e3 H" M
durable complete molecular response might remain in CMR after stopping0 J K3 p4 C q$ O6 j
treatment. Previous reports of patients stopping treatment in complete molecular
9 B# z5 Q4 J! R3 Uresponse have included only patients with a good response to imatinib. We
& d$ @( ]* P, N4 tdescribe three patients with stable complete molecular response on dasatinib/ |* _' Q, B+ w" Y1 Q, B# Q! K2 @
treatment following imatinib failure. Two of the three patients remain in
. |$ w- R6 x, A7 k4 z2 ycomplete molecular response more than 12 months after stopping dasatinib. In9 W! D; }! O9 t8 F1 o7 C% \0 A$ v
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
# u0 \9 X* n+ j- o P7 w' ^' M4 xshow that the leukemic clone remains detectable, as we have previously shown in }, w- [( b2 G4 n: X
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
, F4 P- r" V8 N+ h! Q3 Q2 g8 K' w( Ythe emergence of clonal T cell populations, were observed both in one patient
5 d9 Y5 Y+ r5 p7 ?+ `who relapsed and in one patient in remission. Our results suggest that the
N9 P% H1 H7 Hcharacteristics of complete molecular response on dasatinib treatment may be
% n$ o- ^; z/ J" N: w, O7 b/ psimilar to that achieved with imatinib, at least in patients with adverse
' Q" S+ Q2 B+ [% h, T" Odisease features.
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