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。& S0 C/ G4 |/ a. J2 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。) A$ u2 {, a; B% h
3 f# q1 N q0 d3 X& I5 }作者：来自澳大利亚
% D4 b2 n/ d* ^. O' O来源：Haematologica. 2011.8.9.
: s% b8 D# f$ r0 ZDear Group,; T4 m& ]" G3 @ o( I% e$ C" W
1 j$ |1 S$ k) `4 ^2 PSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
6 A6 s$ Q$ H: h/ otherapies. Here is a report from Australia on 3 patients who went off Sprycel
7 p+ _. z4 }" W# }, ?after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
+ N, P+ C+ R3 [2 K3 ]$ y# sremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
/ q* [, W. ?- [* A7 M2 ddoes spike up the immune system so I hope more reports come out on this issue.0 f& P! ]- p0 @: B
. r/ }6 d( B% s
The remarkable news about Sprycel cessation is that all 3 patients had failed
+ }6 U) i Y; t0 TGleevec and Sprycel was their second TKI so they had resistant disease. This is- p. N0 L0 |. f, z, V, I/ {* W
different from the stopping Gleevec trial in France which only targets patients8 l+ \) s7 N5 E. O3 k- s
who have done well on Gleevec.
( {) a6 R# t! y0 n9 q( P6 J# n( r; b' N9 v' ~3 r) j5 F
Hopefully, the doctors will report on a larger study and long-term to see if the
* X) P, |& d* m1 ]/ D1 R: I6 cresponse off Sprycel is sustained.- K, u; E! {- \6 D+ ]
/ [7 d. ~. z# tBest Wishes,
6 i! V3 Y$ r* o5 ~Anjana3 ^% a; Q; ]1 Y; a" q) L9 t5 b
# t! [- k9 a' \' X0 E1 J
9 b- i4 Q9 c6 L( U) l# J& J
, c* v( z! V* p+ e+ g$ P0 W1 T9 oHaematologica. 2011 Aug 9. [Epub ahead of print]' ~9 B8 M/ @0 k; O% d
Durable complete molecular remission of chronic myeloid leukemia following ?8 X6 m0 R7 G) I9 r8 Z1 D; ]
dasatinib cessation, despite adverse disease features.
4 [' E1 r# t6 ?; c0 J4 s2 GRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.9 i f- O5 \) p5 h) Y, U/ V3 c9 m. @
Source
* R+ l+ p6 Z j' q( }1 Q0 _# _2 DAdelaide, Australia;
! l e8 o0 h1 F; K; L- @
f3 H" ?$ Q+ |4 ]8 sAbstract( i/ E( X, C, |# M8 t7 h1 q5 s- ^
Patients with chronic myeloid leukemia, treated with imatinib, who have a5 f& B, X# G3 d0 V, z; k
durable complete molecular response might remain in CMR after stopping0 P# p' y/ r! \: U% t+ F0 R5 c% ~
treatment. Previous reports of patients stopping treatment in complete molecular
) S+ G. ]* P7 O& L$ c; g+ Hresponse have included only patients with a good response to imatinib. We
' x9 i/ o, j8 n2 u0 odescribe three patients with stable complete molecular response on dasatinib
1 N5 a7 l A: A6 x {3 Ytreatment following imatinib failure. Two of the three patients remain in6 [- u" d+ t, c
complete molecular response more than 12 months after stopping dasatinib. In/ G2 d7 Z+ [1 v5 F. `# e
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
3 R% t" t1 o. P, ?, yshow that the leukemic clone remains detectable, as we have previously shown in
" P* }8 T2 B: g3 J$ timatinib-treated patients. Dasatinib-associated immunological phenomena, such as: ^1 u0 d5 |& r4 t
the emergence of clonal T cell populations, were observed both in one patient
6 v6 b* ]3 v" m' p5 F8 e, ewho relapsed and in one patient in remission. Our results suggest that the
. T, T# N2 | U6 s; y! Z; _: Rcharacteristics of complete molecular response on dasatinib treatment may be
) z+ F$ n7 W0 y7 Wsimilar to that achieved with imatinib, at least in patients with adverse
4 u5 ?% Z$ a N( |disease features.+ @$ X: ]: G& G( r% L Q
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