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。6 w' a' o1 F/ `- R
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。
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( L$ ?* K$ `; \! B4 y作者：来自澳大利亚
# z( K2 W L2 K来源：Haematologica. 2011.8.9.
& B/ g/ M& S. r2 U. xDear Group,
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' m5 z* x; [1 I* R% P" {4 C8 j( g) xSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML& A; Q' a& F5 t7 p% c c! U
therapies. Here is a report from Australia on 3 patients who went off Sprycel
- ?4 U6 X$ f, Y' m% aafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
0 B/ T; ~3 C' B/ Rremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel z# ?8 L* y1 H6 K; j* y; ^4 A
does spike up the immune system so I hope more reports come out on this issue.9 j, ?) L& ~$ H2 V2 H
. Y' ]8 j% y2 M% n! j3 q! JThe remarkable news about Sprycel cessation is that all 3 patients had failed
7 j* a2 A0 K7 |, z% s5 oGleevec and Sprycel was their second TKI so they had resistant disease. This is4 W" \( ^8 n: A( g. D) g- A
different from the stopping Gleevec trial in France which only targets patients( X8 Z, D* A0 }! B, n
who have done well on Gleevec.
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Hopefully, the doctors will report on a larger study and long-term to see if the
& M9 \ H9 j" r& B2 Oresponse off Sprycel is sustained.8 X F# y1 ~$ k% M' t2 U
0 j* O4 w2 @# g- h* G2 k+ u4 o( y4 jBest Wishes," O% F( H. A8 h/ x: p
Anjana
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8 B9 m! a1 ~& X4 p. |1 `Haematologica. 2011 Aug 9. [Epub ahead of print]
0 l+ F. f. ]% z; X$ }Durable complete molecular remission of chronic myeloid leukemia following0 U# W2 v4 L# S; D R) S
dasatinib cessation, despite adverse disease features.
9 Y5 G; b% b8 e' vRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.5 [7 ?7 V) O! J. v$ c
Source
+ q) P( p. T, t. E# bAdelaide, Australia;
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1 T* _! i: u4 D( H$ S! p2 dAbstract
+ U$ l) Q% U4 _2 H4 x; gPatients with chronic myeloid leukemia, treated with imatinib, who have a
7 _2 W5 E6 T6 ?4 m# i6 Y. udurable complete molecular response might remain in CMR after stopping
8 c ~9 w9 E0 M" b+ e+ v: Vtreatment. Previous reports of patients stopping treatment in complete molecular6 s2 S7 V5 b3 |7 I- \* ]2 @
response have included only patients with a good response to imatinib. We
& x1 l8 ] Z3 O% Z4 P, I, ldescribe three patients with stable complete molecular response on dasatinib
, q! p% W" B" i9 mtreatment following imatinib failure. Two of the three patients remain in# \; U; \/ Z5 E% T( D6 c) j9 C
complete molecular response more than 12 months after stopping dasatinib. In# v, M( E1 \# u- a. w
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
' L4 Z& D1 {& E6 pshow that the leukemic clone remains detectable, as we have previously shown in
9 C( U1 J8 k% _- Eimatinib-treated patients. Dasatinib-associated immunological phenomena, such as' I' m* F& Z8 @8 q3 }; }
the emergence of clonal T cell populations, were observed both in one patient
9 H8 u+ s; T0 ?% Z9 O7 n% Owho relapsed and in one patient in remission. Our results suggest that the
9 i1 R; W1 n( V3 o' r$ {" Icharacteristics of complete molecular response on dasatinib treatment may be
0 H* A6 C- U6 w7 J1 tsimilar to that achieved with imatinib, at least in patients with adverse
8 y$ D {. e. k5 a. Edisease features./ z9 r3 H+ ~) u6 u& {# u) g
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