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。, K8 W6 ~' n& ]7 _! F W! N
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。
) W* A, K; _9 \! X1 p. V7 Q7 A : C2 @1 t* y8 j; @+ v
作者:来自澳大利亚
6 u* T4 G! i/ g5 {! z+ R! ]来源:Haematologica. 2011.8.9.
* @; l' Q7 u" b' o& z% X6 B8 \2 d8 `Dear Group,% v6 F; h8 p2 H5 ?% s
3 f1 I- Y# K% D& c0 LSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML$ U/ W. Q9 n0 m1 t
therapies. Here is a report from Australia on 3 patients who went off Sprycel
2 L* A5 S2 T$ e/ r3 \/ Oafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients) g6 H& Y: z: O' T
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel7 k* S8 ~& b3 M+ A' `
does spike up the immune system so I hope more reports come out on this issue.
# ^ ]( C5 L! |
2 m8 u5 b8 E3 R& {% c! Y }& \ }The remarkable news about Sprycel cessation is that all 3 patients had failed
3 i: k$ V/ D" _( ]Gleevec and Sprycel was their second TKI so they had resistant disease. This is
, W4 d3 s' s% a% Ndifferent from the stopping Gleevec trial in France which only targets patients
! w3 m" g3 Q' X M% jwho have done well on Gleevec.
: w& B, I! K' N* y4 H% z
$ Y, L7 x% f- T( D) g5 T! J& SHopefully, the doctors will report on a larger study and long-term to see if the
7 Y- @ Z: j' q& h3 s* X2 l# Dresponse off Sprycel is sustained.' \; n. v e; b: R1 Z
. f& N. X7 X/ U! m. S1 O
Best Wishes,3 o/ i, t0 @# F0 p7 I
Anjana6 _5 H0 R1 Z% l4 s
- m8 w: m4 u" N9 c2 I9 s: F
+ A6 M+ _4 P+ [9 H+ o8 E) K2 s; G5 L$ H+ v8 \" h7 I& `% d. M: Q
Haematologica. 2011 Aug 9. [Epub ahead of print]( E& d% s( e- E& Z
Durable complete molecular remission of chronic myeloid leukemia following
4 ~0 X) w6 | S) Q: |3 Ldasatinib cessation, despite adverse disease features.' s0 a& K: e+ {: Y \
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
- J j$ _( o& |; KSource! c0 s* ^4 ]: g1 O. e
Adelaide, Australia;9 s8 `7 n( U$ z( k( r' h+ `
" z$ U0 f6 ]7 @# Q2 F( \! T0 ~Abstract# y) I5 }. f* R3 f3 I
Patients with chronic myeloid leukemia, treated with imatinib, who have a
% H8 P I, }. t; `' c& Vdurable complete molecular response might remain in CMR after stopping
4 a( m6 o6 o3 {6 ?* \2 xtreatment. Previous reports of patients stopping treatment in complete molecular
# s; l ], w- w" c. O# }' uresponse have included only patients with a good response to imatinib. We
0 ~4 }. N1 _0 @- V/ Q: N: T) G6 V% Ldescribe three patients with stable complete molecular response on dasatinib
. N I. W2 Y* ?& y. ^9 utreatment following imatinib failure. Two of the three patients remain in
( j" B% V9 V3 o) }* {complete molecular response more than 12 months after stopping dasatinib. In& Y8 P' m& e% e5 I* K4 r) H5 E
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
* I$ d6 k0 e( I9 S( ]8 [show that the leukemic clone remains detectable, as we have previously shown in3 V8 N, R4 y3 }; {! W1 H
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
8 V' M" d% C3 Xthe emergence of clonal T cell populations, were observed both in one patient$ D+ _5 G: p& S7 @; p& L; r
who relapsed and in one patient in remission. Our results suggest that the
! y+ o: ^2 x' x$ n- l d% m' s- Z& y tcharacteristics of complete molecular response on dasatinib treatment may be( P6 n V$ l% m8 {$ Q
similar to that achieved with imatinib, at least in patients with adverse
" ~0 r- W6 T- i! D: B# Q3 [disease features.
" [# a. ]( g) B2 x |