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。
4 ?3 q5 o$ F4 {% d! L- U" b! 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。 c* z) a; _/ W2 i: p
; H x& A" H# |作者：来自澳大利亚2 V) p, H$ d$ n" m
来源：Haematologica. 2011.8.9.5 b& x* {" K7 O1 M# a
Dear Group,7 W: i0 F8 O+ J1 m
& I. [7 q+ M9 j; M" I7 GSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML8 {( C2 v$ V3 U0 U+ m$ G. z2 I: U6 K
therapies. Here is a report from Australia on 3 patients who went off Sprycel1 c. q& \% b! V2 A
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
0 z& q4 w' y. }% r5 A8 o/ y% Aremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
- |; [0 o1 _) K+ x$ j$ x- ^9 {does spike up the immune system so I hope more reports come out on this issue.
+ U6 q9 ?) I$ q7 [# \- q
) X6 R; o ^5 w6 qThe remarkable news about Sprycel cessation is that all 3 patients had failed$ L' J/ D- z; w( Q) y
Gleevec and Sprycel was their second TKI so they had resistant disease. This is5 ?# O( E! R9 O$ a }7 U
different from the stopping Gleevec trial in France which only targets patients
; P t' ~7 {' C/ x9 y1 w/ S/ b4 g4 uwho 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
' R' Q G6 D. }# Y V5 z/ nresponse off Sprycel is sustained.; R3 ]: O8 S0 b
4 E2 t+ W' k1 V$ nBest Wishes,8 M U l( V8 F
Anjana- }, p. c7 S6 g/ a4 G# M8 v* }9 P8 e! |
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% u) J( W" ^& n+ l2 `, J
) e: [0 R+ P6 \! X( J. ^: Y, IHaematologica. 2011 Aug 9. [Epub ahead of print]8 G7 ]7 ^6 ?2 l8 C1 w# \$ T5 j
Durable complete molecular remission of chronic myeloid leukemia following
7 K; s$ h( |$ `! hdasatinib cessation, despite adverse disease features.! Z* l5 U! Z' P B# X! }+ ]. _
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
1 j5 M: F* Q( t& X5 M3 L" [1 eSource
% A6 ~) B* \: R* v4 EAdelaide, Australia;
8 u2 u. P! G% V7 o' q
( F+ A8 n- J* B+ z+ E* cAbstract
" X0 W# l0 K# U9 Z6 GPatients with chronic myeloid leukemia, treated with imatinib, who have a
, R3 l- D! O) Y6 ldurable complete molecular response might remain in CMR after stopping' j2 E7 t: X! N5 r; X6 q
treatment. Previous reports of patients stopping treatment in complete molecular
4 k( u% s/ |$ {, J3 presponse have included only patients with a good response to imatinib. We) T2 o+ T- S& r. q4 T* w& `7 t W
describe three patients with stable complete molecular response on dasatinib2 l) ~; e2 F( f
treatment following imatinib failure. Two of the three patients remain in
& B' H. L2 ^, C% c+ Pcomplete molecular response more than 12 months after stopping dasatinib. In/ H. q% Y2 u' \5 Q
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
p- N& H& g. V4 ~6 xshow that the leukemic clone remains detectable, as we have previously shown in3 Q+ _5 I5 O0 Y5 P: p2 }
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as; v+ S/ P& d* J: X* D% y- _. N
the emergence of clonal T cell populations, were observed both in one patient
! v. I; D6 p6 Pwho relapsed and in one patient in remission. Our results suggest that the
a& W3 v1 \7 lcharacteristics of complete molecular response on dasatinib treatment may be4 `3 l- t) a9 {/ Y
similar to that achieved with imatinib, at least in patients with adverse1 p0 S4 |. b' T
disease features.
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