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。. b/ R1 j4 u2 A s1 f
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。5 k2 U1 h# R$ _, l
4 |, t8 U# p* t! ]: f4 n& `% o
作者:来自澳大利亚
0 {' ?2 D3 [+ Q( e! n7 ~来源:Haematologica. 2011.8.9.
! w. P8 Z. y- N- O& EDear Group,% P; F6 i B& t( _4 Z6 R# ^& r% U
& ~8 P3 h( u7 V5 W- q" m# p
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
8 |7 a3 o2 D) K# v# ctherapies. Here is a report from Australia on 3 patients who went off Sprycel% D5 p; |: D5 f. I; T
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
$ b% t5 g- E; s, ^! v/ Hremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
" C& L& k6 N5 a m6 }does spike up the immune system so I hope more reports come out on this issue.6 w2 w6 ^6 A ~/ i$ p0 I# U
0 j6 V; [- @' ^- t( fThe remarkable news about Sprycel cessation is that all 3 patients had failed
) Z3 {7 K5 E* @6 V$ @. `; y% F6 zGleevec and Sprycel was their second TKI so they had resistant disease. This is7 z4 L a2 `; p! R4 \' o( I( l& R
different from the stopping Gleevec trial in France which only targets patients
9 _/ d$ {! t6 X% |( K# \( n4 Kwho have done well on Gleevec.8 P2 l3 t* |9 i" M/ D q2 E
% _# p& Q( B1 R
Hopefully, the doctors will report on a larger study and long-term to see if the
' K5 R! C6 `7 Vresponse off Sprycel is sustained.
# x) h% y2 r. G
' [ j6 F( z' I% Y% y# F- }Best Wishes,% w' U9 a3 p4 l+ E6 Y* l
Anjana
3 b& c0 L. C4 e6 J0 m4 _8 e
5 {2 h7 E5 n6 o: B' Z/ j% Y* V+ n
: h. f4 t7 V: t
8 b1 |! [$ g) KHaematologica. 2011 Aug 9. [Epub ahead of print]
. F3 ^- L" b# u3 c d1 VDurable complete molecular remission of chronic myeloid leukemia following2 S6 V% ^; l9 p" k% @
dasatinib cessation, despite adverse disease features.
! b% c' M/ r1 }7 cRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
u+ Y: u3 B3 @% Z6 T) G2 ^, r- mSource2 x! o+ P: e- j* w) j2 [! |5 O
Adelaide, Australia;8 a+ x8 P- P' T+ u! n
( F; T. B/ `6 ~' [0 P2 QAbstract) y4 y" E, v7 @9 m
Patients with chronic myeloid leukemia, treated with imatinib, who have a0 u/ i( N: m( F9 P5 _- p& l4 ^8 I8 ?
durable complete molecular response might remain in CMR after stopping8 I+ b# J4 Z4 V. u/ N
treatment. Previous reports of patients stopping treatment in complete molecular% x3 ]5 I1 y$ A" a4 Q! L
response have included only patients with a good response to imatinib. We
2 ]4 o. b1 `2 m. p1 L; x Vdescribe three patients with stable complete molecular response on dasatinib
( M; p, F( [* \8 u$ c- ytreatment following imatinib failure. Two of the three patients remain in
! u5 P/ e( X+ ]. s" U7 s: }$ ]complete molecular response more than 12 months after stopping dasatinib. In
* r, u* i$ T0 E. a( hthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to* \" y! e$ N" l, q
show that the leukemic clone remains detectable, as we have previously shown in A2 V# I" G5 @4 h7 V7 G( }
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 ~6 P/ \( F- H' W" B; @9 k% C$ wthe emergence of clonal T cell populations, were observed both in one patient j/ F3 M+ a0 n4 {
who relapsed and in one patient in remission. Our results suggest that the2 [4 Y( p, ~8 E3 T/ E" X% }# |
characteristics of complete molecular response on dasatinib treatment may be3 d2 @9 w# L/ ^ M0 ?" E* n0 ?
similar to that achieved with imatinib, at least in patients with adverse* ?4 d$ I: A/ ~ g
disease features.
5 X( p2 s1 U7 c# D6 v* j5 g |