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。5 l9 D5 X; a' M, }
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 S ?! R8 i4 {7 |5 B
0 _# {6 ?6 a) O2 \8 `1 j作者:来自澳大利亚
8 ~- ` K7 n- N; q$ {/ g来源:Haematologica. 2011.8.9.$ f# ~6 r' c* F1 p$ r
Dear Group,0 {* c- z# S! ~& a
4 R L; ?) f( @! S
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
' e8 a& G1 Y! U2 G T1 Gtherapies. Here is a report from Australia on 3 patients who went off Sprycel8 Y+ b5 b& R* O
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients( Z* k: o2 a( g: i/ A% d
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
6 e0 { S- G7 q1 L' Jdoes spike up the immune system so I hope more reports come out on this issue.
# Z4 }- }0 y5 m& u4 ]7 D. S
3 P. j7 D9 l) z& n$ w# K( y! xThe remarkable news about Sprycel cessation is that all 3 patients had failed
. O1 Q- j9 @" [" a6 I1 \) h- ?Gleevec and Sprycel was their second TKI so they had resistant disease. This is0 [% h. P8 r. Q5 u5 q% D
different from the stopping Gleevec trial in France which only targets patients& q' y& s3 K5 x4 q. m
who have done well on Gleevec.3 e& `. u9 F/ C" s: A9 A/ L: S
1 L8 ^$ m+ i( f+ y& qHopefully, the doctors will report on a larger study and long-term to see if the) `, ^. J# z/ K$ W5 L8 M3 S G$ i
response off Sprycel is sustained.9 `5 X8 ~$ N, E4 O2 p
7 @$ N) L, Q! }- ~2 _! C" JBest Wishes,$ _: q5 f! B' p) F" }1 j/ B
Anjana! c5 X' X( ^+ e0 O2 H
' i& H& d* v/ }1 j J+ E: S# f8 f, a: L* T" ~" s
, N4 t" D$ e% x* R- N5 ] [
Haematologica. 2011 Aug 9. [Epub ahead of print]1 R2 L7 M% G! [+ A" ~% f
Durable complete molecular remission of chronic myeloid leukemia following/ c: B6 L* y; q0 n8 @
dasatinib cessation, despite adverse disease features.
2 [' y% P+ m) K+ F$ [4 i- dRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.* t' c$ S. c6 t3 ~0 L
Source! K3 O6 l* b# Q
Adelaide, Australia;' l4 |* g, a0 X7 U+ c
' L, M+ z5 y. t- I; [6 H1 ^* DAbstract
- U% C/ W& n) z5 F2 s1 }2 r3 O( r9 X0 [Patients with chronic myeloid leukemia, treated with imatinib, who have a
0 T' b3 D8 V9 a1 I0 B: h- N, a" J0 o1 Edurable complete molecular response might remain in CMR after stopping9 k; G8 M( o! V( f! d$ C0 |3 q
treatment. Previous reports of patients stopping treatment in complete molecular
8 \8 `9 g. U! w* W* `7 c0 A# Wresponse have included only patients with a good response to imatinib. We( V( c+ v r. _3 L: [- ^- T9 B
describe three patients with stable complete molecular response on dasatinib
! O# f+ g/ D6 U( |8 s8 Btreatment following imatinib failure. Two of the three patients remain in
. Q' K3 ]" b7 N1 Wcomplete molecular response more than 12 months after stopping dasatinib. In7 E, [' S7 c3 C# Z7 e' p; }
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to' J2 P4 {* V! l* n* y- n! S
show that the leukemic clone remains detectable, as we have previously shown in
# P! I4 }& ^! ^imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
% }3 J. V2 [8 }3 othe emergence of clonal T cell populations, were observed both in one patient
3 J, f" U8 Q% y1 M, e! ewho relapsed and in one patient in remission. Our results suggest that the1 ]( Y7 n& O& C5 K7 N3 P
characteristics of complete molecular response on dasatinib treatment may be
' K& m$ \$ [, }$ Vsimilar to that achieved with imatinib, at least in patients with adverse
8 H6 u" J8 e2 z% I" i+ hdisease features.' X: c. h/ L& n+ {
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