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。" _# r. E- u; R- b: t( \- ^, y
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。4 t3 k0 u1 a' n0 m ~' Z
: O" V( P/ N" m0 d: R' E+ Q
作者:来自澳大利亚! z* D* L- o; `. K; U: p! U
来源:Haematologica. 2011.8.9.
% X& F% b i7 y# Y/ jDear Group,2 R% g1 I2 q/ H @' P7 T) V$ P
e, p3 u/ {+ ]
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
, c& N" N! C, f! ^therapies. Here is a report from Australia on 3 patients who went off Sprycel
* |9 q: p/ b! i3 ]( p/ Uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients' t" h; J8 t) h3 l# C/ ~
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 Z/ ^ h# h+ ^7 Xdoes spike up the immune system so I hope more reports come out on this issue.
* X4 f& c2 u6 a5 l8 {5 h$ F3 e6 \; k3 K) q7 u4 w5 n3 I# ^
The remarkable news about Sprycel cessation is that all 3 patients had failed4 c i- f' U8 A) C$ h
Gleevec and Sprycel was their second TKI so they had resistant disease. This is9 C9 s2 N. d/ f
different from the stopping Gleevec trial in France which only targets patients
- d& [; @% N$ G. v' }$ J; xwho have done well on Gleevec.
3 [& d; W6 S/ O
8 C: O7 m/ ?+ B2 zHopefully, the doctors will report on a larger study and long-term to see if the" o R6 b5 r: {4 [0 C3 H
response off Sprycel is sustained.
, ~3 ~* C6 n& }) S5 B- {! b2 ^' c
: y+ J. F7 x0 {9 qBest Wishes, X/ ]/ {5 [# M9 ~% A* f
Anjana
4 r/ |6 t4 b( ^- `$ Y5 R2 Q+ O% q: k: R
; S5 \0 M# ~+ B1 J) H$ G* D" i; c/ c$ b, B6 L0 _
Haematologica. 2011 Aug 9. [Epub ahead of print]3 Z0 V9 q6 q: s7 w# r; ~& g
Durable complete molecular remission of chronic myeloid leukemia following' \2 R% n2 r, @! ^4 A0 S. P
dasatinib cessation, despite adverse disease features.+ A5 v0 M5 U5 \) h6 r0 D, @, u* h
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.# Z" G! n/ }2 m* Y* D
Source
0 G m, D$ N( v6 m1 u, AAdelaide, Australia;
( W. @% A# {, w4 G5 _. l+ @* z: t |1 [1 z" H8 a0 C9 c1 A# a
Abstract9 ^' Q% k D2 }/ c
Patients with chronic myeloid leukemia, treated with imatinib, who have a) `, {! M( ^7 d2 x& a( }& \
durable complete molecular response might remain in CMR after stopping' d# M* N9 I5 H. R
treatment. Previous reports of patients stopping treatment in complete molecular- W/ E2 F# p: S
response have included only patients with a good response to imatinib. We
+ m5 k7 O& n( `, c1 o9 edescribe three patients with stable complete molecular response on dasatinib2 m6 `$ \$ E9 a9 i
treatment following imatinib failure. Two of the three patients remain in4 i. w' j5 j) _* c4 C( [
complete molecular response more than 12 months after stopping dasatinib. In; l+ T' d0 V& B5 U& ?
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to& K3 t) Y. u4 X2 u; X2 R. D
show that the leukemic clone remains detectable, as we have previously shown in
: ]8 p7 x7 ^3 h R! n& [) \2 Oimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
' F7 d8 C8 B! y! |% b: F- g( Tthe emergence of clonal T cell populations, were observed both in one patient, ]) O% y7 [3 O0 \
who relapsed and in one patient in remission. Our results suggest that the5 K( v/ E& e) e& K7 M' T
characteristics of complete molecular response on dasatinib treatment may be
: ?# Q8 \# j: A' u$ p/ Y9 S- wsimilar to that achieved with imatinib, at least in patients with adverse
# p5 j$ G9 g( q/ t5 F7 _6 U6 _disease features.
6 J- R: j+ B: ? |