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。- Z" M: Q/ j% g2 _6 a4 \0 Z* _
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。
& K6 L- M% g! i4 ?
, H3 B1 f }" S2 s# o: e w5 k作者:来自澳大利亚$ U, p& x N" ~& d, H
来源:Haematologica. 2011.8.9.1 |/ \* K/ J' [% E* `! X9 C& P6 N
Dear Group,
* n [( _$ Y8 k; m: ^- o6 ~5 M5 w; }( r
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
! w& T5 w$ J% ?) M; ]4 w7 k$ }therapies. Here is a report from Australia on 3 patients who went off Sprycel1 B/ ^9 C0 s% Y7 }
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients7 }8 {5 C+ q% D) }$ S* S
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel) }- v8 {) k# p2 p
does spike up the immune system so I hope more reports come out on this issue.
' s# G ~ Q* z3 O( p6 T" _- l/ \% K( K
The remarkable news about Sprycel cessation is that all 3 patients had failed5 T3 M5 [( _1 R6 Y. G3 C2 ~
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
& `. W( e) R. U* q6 Z# O: \$ M/ Ndifferent from the stopping Gleevec trial in France which only targets patients
! R7 N2 }3 P3 C5 a6 dwho have done well on Gleevec.
7 e3 O9 I0 K5 h0 R! Q0 p- L
6 k/ m& a0 i, {" Y3 M) w1 M* XHopefully, the doctors will report on a larger study and long-term to see if the6 L' C. z3 t6 A
response off Sprycel is sustained.
% Y% t7 T# ?' X# p2 Y! z" V
+ e1 Q% `- _7 g% i" r. WBest Wishes,
) o: j9 A5 A) e6 yAnjana
6 m) X n. i3 c$ l
- K9 N% i8 I, N8 m) J; a: O* L5 V" R. Z2 k- s1 Y- A- I/ w
4 c; \ u4 I! G" ~Haematologica. 2011 Aug 9. [Epub ahead of print]
( @# l! [% @5 }$ ]Durable complete molecular remission of chronic myeloid leukemia following
i% A* M% `/ }" I8 zdasatinib cessation, despite adverse disease features.. {& t- Y7 |7 K, H' C
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP." V* O! N/ w) c! r
Source
8 I. z6 f, m5 X/ zAdelaide, Australia;* b" m a3 U, f- J( o! Y: i
" V* F; n! t; v2 p2 L/ mAbstract
! r/ R | Z: s% S' r1 f" xPatients with chronic myeloid leukemia, treated with imatinib, who have a
$ K" p, c% Q0 y( W2 odurable complete molecular response might remain in CMR after stopping) v' J( d8 `- y3 F% i& f! @* Q* r7 E0 Y
treatment. Previous reports of patients stopping treatment in complete molecular U3 ?/ b+ b. _3 R8 ], w
response have included only patients with a good response to imatinib. We
4 r$ z: Z6 L4 Z" Wdescribe three patients with stable complete molecular response on dasatinib; s) [7 A3 B6 I1 L! F# Y
treatment following imatinib failure. Two of the three patients remain in
; }$ b, _/ R1 m0 m9 Ycomplete molecular response more than 12 months after stopping dasatinib. In! }$ O; P# O$ f4 k
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to4 \: A- A& P; P5 [
show that the leukemic clone remains detectable, as we have previously shown in/ A( ~- |$ [# P- k; p. j6 _
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 V: A2 G) A8 E- l3 wthe emergence of clonal T cell populations, were observed both in one patient0 X. G( J$ V" e, T- K, U4 z
who relapsed and in one patient in remission. Our results suggest that the0 m9 j; ?0 _- \. ~. \% b& |8 D
characteristics of complete molecular response on dasatinib treatment may be" V, }3 ?: M( \
similar to that achieved with imatinib, at least in patients with adverse
6 p- r: m |* q, ~* o) Edisease features.
0 p/ `; l" L) C7 Q1 `; @ |