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。/ W1 V" K E, C
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。7 b5 e; {3 P" ] |6 E9 _
2 w2 v/ q, }- C: a4 r+ p" S5 k! q) ~. N) Y作者:来自澳大利亚5 }0 u. Y& Y/ _# d$ d7 u! z& k
来源:Haematologica. 2011.8.9.
V* C, i3 F* c2 `+ ?$ b9 d: vDear Group,8 A4 i* V9 }: L3 k. S
4 m* b, I2 v6 O( U0 m" @* H/ ]Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML7 P& ?, X" R7 L+ B' r" k
therapies. Here is a report from Australia on 3 patients who went off Sprycel
% v- {3 x, _" p7 f3 uafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients. T, j2 `$ l1 z+ h8 F* L1 x
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
% T& b2 T) Y8 m" E& s9 pdoes spike up the immune system so I hope more reports come out on this issue.( o6 c7 f& X- t0 U, c
/ T F, s+ {. Q. {7 I0 J+ i/ sThe remarkable news about Sprycel cessation is that all 3 patients had failed
B5 i% P( E+ r! |* f; W$ u h" \6 TGleevec and Sprycel was their second TKI so they had resistant disease. This is2 I: l, p+ N* L y/ t- Q
different from the stopping Gleevec trial in France which only targets patients- d! x2 M: H* Q7 R Q3 ^" j- A- Y7 x
who have done well on Gleevec." | F- r" `: `
7 z+ r3 C) s2 l: eHopefully, the doctors will report on a larger study and long-term to see if the$ N* E9 n& \1 ^, O" c2 q
response off Sprycel is sustained.
5 o1 }! R0 E: m/ z
, ?+ W- l$ O$ O6 p: GBest Wishes,
4 r6 D( Q! p7 X6 PAnjana
7 g/ J6 m3 m6 x* K4 r6 `- ^
! H/ E2 ]# u1 Z$ A3 ]. g6 }6 ]7 _3 }1 b$ n7 V* D5 ]" C$ `1 @& y
9 {! R1 j, ~* @* r3 yHaematologica. 2011 Aug 9. [Epub ahead of print]
9 C7 j/ ?8 h0 L# ~" e! dDurable complete molecular remission of chronic myeloid leukemia following
9 {4 G8 h8 a$ e; ?5 I: V: ^dasatinib cessation, despite adverse disease features.
! Z: {! l0 P$ z( ARoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
m0 C# j3 \0 kSource, ? H5 U" {; K$ B9 c
Adelaide, Australia;
4 G/ U' R9 q+ D* n. f& B+ T* T. K1 W8 Z& @# B
Abstract' t# c; Z4 `1 A2 C
Patients with chronic myeloid leukemia, treated with imatinib, who have a( V. c5 U( K- M6 Q3 b P
durable complete molecular response might remain in CMR after stopping0 K' \; s6 s. i3 w# B7 v; P
treatment. Previous reports of patients stopping treatment in complete molecular/ V: [2 x1 L) X0 e
response have included only patients with a good response to imatinib. We
4 h- X, q2 h/ N+ ~* ^describe three patients with stable complete molecular response on dasatinib: W( g4 X v" e" S- h# D7 ~5 u
treatment following imatinib failure. Two of the three patients remain in4 \( X) x# f1 x- c# m1 l9 k! ^
complete molecular response more than 12 months after stopping dasatinib. In6 |$ g3 z& q" w0 v: Q: @
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to( s& |; y( }& S. {6 b
show that the leukemic clone remains detectable, as we have previously shown in
7 U6 X; Y0 v/ a$ q; X: G) Eimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
H, Q; E4 n! A0 p% `the emergence of clonal T cell populations, were observed both in one patient9 j: e m. I, T3 Y
who relapsed and in one patient in remission. Our results suggest that the
; S- v! x0 h: V% s. tcharacteristics of complete molecular response on dasatinib treatment may be
) V, z/ V# I. W4 w; fsimilar to that achieved with imatinib, at least in patients with adverse
; q- u/ X/ H! J/ L& b! kdisease features.6 _2 R8 ~' r; ]8 j# E
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