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。
* L. [& {! A0 T: a! K 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。+ Y9 x8 ~; v5 N0 E) `
& P" T5 i' b3 v6 v作者:来自澳大利亚
3 N7 p+ C( o2 J来源:Haematologica. 2011.8.9.
+ P! j9 ~5 j+ }# g$ `Dear Group,
# ?# `1 K% D( V2 B2 W2 e+ g8 C5 ~$ c. _9 l
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
' U' S8 a8 k ^7 a- }therapies. Here is a report from Australia on 3 patients who went off Sprycel
0 D1 ?* A3 m1 y& e! I6 g' ]after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
1 O3 \2 v+ M$ Wremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel# `# B) ^$ b4 c! l6 L6 `, k
does spike up the immune system so I hope more reports come out on this issue.. J" r& u: a& `; M( D2 @
" M4 M* E t9 m5 |$ HThe remarkable news about Sprycel cessation is that all 3 patients had failed
6 C5 F6 D9 a: I P1 }# T5 BGleevec and Sprycel was their second TKI so they had resistant disease. This is( g7 A( o% _" N3 P
different from the stopping Gleevec trial in France which only targets patients- d9 k2 d C% k' I* X( I/ A5 {+ c
who have done well on Gleevec.
4 j/ j4 B4 j L a5 x8 Q9 S6 y/ [$ y' ^' e( O3 Z: }
Hopefully, the doctors will report on a larger study and long-term to see if the* f: N0 N; o( W! A
response off Sprycel is sustained.8 y/ p4 {+ h v& w: Z$ X, o
; G& e" F8 c' u8 k' }3 T
Best Wishes,! x* F! |$ x5 C5 L# A( O A
Anjana
# ^& T! z; F$ ?! N) V0 K7 U5 ]* q# K6 F) _5 C
, L% ? l. i& d! F! O1 N+ ?
$ M+ x: |& U$ H4 c+ B3 o/ g6 u' `, W6 {Haematologica. 2011 Aug 9. [Epub ahead of print]+ l$ b! H. N$ T! L& U4 c" S4 h" q+ x
Durable complete molecular remission of chronic myeloid leukemia following
/ [$ i9 D1 ~; j I j0 Zdasatinib cessation, despite adverse disease features.
2 K) `4 V' @$ m% C" D. rRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.) y( H& g. {# }9 q8 x( ?$ r
Source
- O2 m G2 ^ j5 Y$ J; _3 S: |Adelaide, Australia;
9 L/ I+ O% t, G- t0 i: L
* z/ V; C4 O2 P. g# z! Z2 {( E" FAbstract/ l/ _" a' i9 {/ r3 y
Patients with chronic myeloid leukemia, treated with imatinib, who have a M. q# s) S! x; N( Z
durable complete molecular response might remain in CMR after stopping! T! m+ |2 M1 I( x- n# Z
treatment. Previous reports of patients stopping treatment in complete molecular
, }- Q! S+ [4 Z H' ^response have included only patients with a good response to imatinib. We
" f* B0 u ~( {: T7 j2 l( n+ V0 Adescribe three patients with stable complete molecular response on dasatinib
: P p; @9 L$ c: ?* wtreatment following imatinib failure. Two of the three patients remain in
! ^2 E! f1 h5 X4 j4 ?% Acomplete molecular response more than 12 months after stopping dasatinib. In
* w, \; O2 w9 @& u) M; d7 \# lthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
2 j" R4 e0 N. cshow that the leukemic clone remains detectable, as we have previously shown in) A. |! a* Y+ v8 N3 r
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
& P2 I' n% n* ]7 p+ ethe emergence of clonal T cell populations, were observed both in one patient$ S. S: F1 v- P; I+ Q- g- c
who relapsed and in one patient in remission. Our results suggest that the" E9 g! o( `0 u
characteristics of complete molecular response on dasatinib treatment may be8 r1 z1 [5 Z4 u" g, J* i# v! P
similar to that achieved with imatinib, at least in patients with adverse3 F& m+ a ?+ q4 l# V) C, Y
disease features.! }8 I0 I' u; k/ @9 q
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