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。1 ^! }: d" c% ^* W3 @
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。% X7 Q$ C$ `5 S- j# v. D
& _( `! i: G2 i9 B作者：来自澳大利亚" p) _) G: l1 o% _9 u0 m# g
来源：Haematologica. 2011.8.9.
" |$ e6 Y+ P) E+ h3 {; ^( `2 gDear Group,7 b; l7 q* _0 w* ?0 {: `% @0 x4 L
6 U3 E% }8 Z: M* J
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
3 v6 A- T) h1 N# d2 ?; ]/ etherapies. Here is a report from Australia on 3 patients who went off Sprycel4 C. U5 _$ a- w, u# \3 j" _( n
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients a7 X9 T2 |* U/ n8 S6 Y0 V
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
/ P: m9 n( B( v: d- H! U! Kdoes spike up the immune system so I hope more reports come out on this issue.6 t" s9 L* p# H& ^# I+ C( ^
% ]! b3 x& Q; Q* @( B
The remarkable news about Sprycel cessation is that all 3 patients had failed
( Q# @) |6 y4 z! j. J7 h, LGleevec and Sprycel was their second TKI so they had resistant disease. This is- i8 `$ [' F! h$ x( Y
different from the stopping Gleevec trial in France which only targets patients
9 |1 B4 m0 ~% j3 f. s3 vwho have done well on Gleevec.6 Y9 w4 }+ F/ y+ j4 u2 T9 g8 o
" _% v# d. P" K( p: s
Hopefully, the doctors will report on a larger study and long-term to see if the
' {, L0 Z3 i7 u/ n" a+ F; k! y5 rresponse off Sprycel is sustained.
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9 f6 d) P8 u" V% B, oBest Wishes,
! i; D) F" G+ H. D* CAnjana, @4 h. Y6 f$ ^. W R( L
) U t& r5 E: J6 Y3 {5 X+ L8 _& w4 a: M3 A. A+ i9 T% Z) J
8 X# R: |2 v8 QHaematologica. 2011 Aug 9. [Epub ahead of print]. I9 r& j. G# _% s9 D9 V0 s
Durable complete molecular remission of chronic myeloid leukemia following
) |6 d5 X& |; cdasatinib cessation, despite adverse disease features.! W* u: y2 A7 \6 J( \0 t
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP." i- ?" [% O9 ]/ C
Source) X% ^; R. i s7 T# @! @3 S
Adelaide, Australia;
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6 ]( m0 K; ?3 @6 d+ QAbstract6 g s4 H k1 f/ A: @* P# \1 n& s+ K& [
Patients with chronic myeloid leukemia, treated with imatinib, who have a
' E; V. }" ?6 d6 E0 d; R* v2 Rdurable complete molecular response might remain in CMR after stopping9 ^+ A/ c4 @! w5 m8 G6 x( z
treatment. Previous reports of patients stopping treatment in complete molecular
" m. k2 w5 d+ N. j8 rresponse have included only patients with a good response to imatinib. We
: r; n7 w* D6 x/ G1 [: R( fdescribe three patients with stable complete molecular response on dasatinib( k4 D/ n, `$ Q1 o
treatment following imatinib failure. Two of the three patients remain in+ n; q2 X* b9 E$ |: |* G+ @
complete molecular response more than 12 months after stopping dasatinib. In5 q: B8 }& h+ s! h$ S0 }
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
( ^7 ]1 U3 j1 {( @show that the leukemic clone remains detectable, as we have previously shown in
/ A- U3 U6 M4 |" l* Timatinib-treated patients. Dasatinib-associated immunological phenomena, such as0 L' A% S) e7 a2 N
the emergence of clonal T cell populations, were observed both in one patient5 R% K- a" f) `/ ?* z
who relapsed and in one patient in remission. Our results suggest that the$ ]+ N" O" F# o9 s
characteristics of complete molecular response on dasatinib treatment may be
1 R$ k) r* f3 }, hsimilar to that achieved with imatinib, at least in patients with adverse
+ c5 V' g* | M, M3 F( t; T, Q- V2 Hdisease features.) {+ Q$ @7 d* L$ X1 a
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