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。' t6 H0 X- d, q6 Y7 W$ w9 n% O
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 h& z0 q0 U) Y7 Q& h5 W/ Z
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作者:来自澳大利亚
$ e$ d# a; D8 A- J, z/ v来源:Haematologica. 2011.8.9.! x( Z4 N8 d2 ~* S. V& X; O
Dear Group,) k4 ^, u' x& y3 K; D5 @
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML! i$ [ p1 B3 Q# M, B4 y1 |
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 v/ v5 O% M9 v! I
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients& ]! q) G7 G6 s4 v1 V+ U
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel" i. ^4 v T; j& A
does spike up the immune system so I hope more reports come out on this issue.
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6 ^$ R1 n0 `# E9 R8 r$ J& ~9 hThe remarkable news about Sprycel cessation is that all 3 patients had failed) b3 K) i5 J* q
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
( P" |& Z2 f4 j, H6 B2 {3 y* tdifferent from the stopping Gleevec trial in France which only targets patients% ?8 D; Y& `9 ~% t- |
who have done well on Gleevec.2 }5 W2 M0 M" R' X6 w6 a5 N2 E
. C2 _ S$ v) T" UHopefully, the doctors will report on a larger study and long-term to see if the
& d" u. {- P, ~0 xresponse off Sprycel is sustained.
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Best Wishes,
1 \: e% h( m" U3 TAnjana1 p4 E3 N. X* M3 G5 K I; C
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/ s) x, Z/ d2 K8 ^! pHaematologica. 2011 Aug 9. [Epub ahead of print]( ^' O S o& n* P- J
Durable complete molecular remission of chronic myeloid leukemia following
/ h( r6 |8 F* vdasatinib cessation, despite adverse disease features.6 l* |, z a w7 f2 N1 t
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.7 W# E" h& A7 x8 h
Source
- Z, j& {( r. P! PAdelaide, Australia; c; W0 v5 c% p+ c0 U2 N
% E) {# ]) P' G0 l5 ~) jAbstract
7 S$ C7 a% S0 _7 U5 QPatients with chronic myeloid leukemia, treated with imatinib, who have a2 P: F/ A2 g8 `5 b' J! _
durable complete molecular response might remain in CMR after stopping
. x" L$ W6 \1 M, a/ V; I6 X' [treatment. Previous reports of patients stopping treatment in complete molecular
4 I5 ]: a* T& G0 C! Qresponse have included only patients with a good response to imatinib. We) S+ E9 C& ^- j9 i( F2 k3 f
describe three patients with stable complete molecular response on dasatinib
2 b! b) Y* i$ W- g; l3 m- otreatment following imatinib failure. Two of the three patients remain in
- }8 n; {3 q% Wcomplete molecular response more than 12 months after stopping dasatinib. In
1 {: i& L3 l4 m3 F7 c! ]/ mthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
. {) x3 U, H: u$ f5 w. ?show that the leukemic clone remains detectable, as we have previously shown in
+ q3 B# Z( G0 K# A5 h4 Vimatinib-treated patients. Dasatinib-associated immunological phenomena, such as# \; O4 o/ P* P2 L! e
the emergence of clonal T cell populations, were observed both in one patient
* M7 R* Q8 y! t$ X# ~5 ^* pwho relapsed and in one patient in remission. Our results suggest that the3 x6 u' g( z \( e
characteristics of complete molecular response on dasatinib treatment may be
! e$ |0 S* q h/ m; z& K; V3 ssimilar to that achieved with imatinib, at least in patients with adverse
; b( b+ y( |) _! s. e( K( jdisease features. L( e% v; b5 Q, K" o2 ?) G8 r j
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