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。" B+ A5 G6 u* m0 L, g8 T F0 J
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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3 G; B7 x5 {0 E/ Q u; Q作者：来自澳大利亚7 _. l( P7 G8 b3 h7 Z) m! b5 l
来源：Haematologica. 2011.8.9.% l: P! F( ]0 R6 l* ^& h
Dear Group,) S m5 x3 i% k4 F# S% N- \
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML( H, h. ^! T x% D4 Y
therapies. Here is a report from Australia on 3 patients who went off Sprycel
4 |) `: h6 R0 [' |4 Dafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients) z7 y4 ^, p, C& v" i; q
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
1 o- L1 M1 l( K7 F- [; ?3 x0 p5 mdoes spike up the immune system so I hope more reports come out on this issue.
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+ |" \. B7 L+ ~! @. H6 r6 @- J% ]The remarkable news about Sprycel cessation is that all 3 patients had failed, Z2 g& i0 ~& ]/ H
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
- n+ y: Q% Y' e* ddifferent from the stopping Gleevec trial in France which only targets patients
3 L. q, J4 m6 |& K+ W4 Hwho have done well on Gleevec.5 r0 n. X4 v) s% i2 T: n1 P2 J1 j
1 n/ q# _" P1 K/ x: j9 S2 RHopefully, the doctors will report on a larger study and long-term to see if the
1 [% R( ?2 I2 \, [- E7 l6 ~% _response off Sprycel is sustained.# }* L9 ~- `, y3 d
5 |1 a% \4 I% F1 {5 G2 i V( `7 d
Best Wishes,' G" Y: n8 F) D
Anjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]3 w2 r9 A7 y: A% \) x/ N% s/ _
Durable complete molecular remission of chronic myeloid leukemia following6 b7 ~+ `' g3 d+ a9 ?- m
dasatinib cessation, despite adverse disease features.
; _ ^! k8 A" s7 U" z \4 kRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.1 u* J' j/ Y! t. i7 F
Source
7 Q( _- P, ^0 d) B, C1 LAdelaide, Australia;& M- e2 J" a0 X$ ?( q# R; K) A
6 Z U2 w' _; V; G! R! ?! ]Abstract
' \9 b" b. o2 X5 U( M- `$ _/ Z# ?* |Patients with chronic myeloid leukemia, treated with imatinib, who have a
3 f# w& h% O" ^3 I, Udurable complete molecular response might remain in CMR after stopping. J- R1 ^" v) P+ s4 p( Q) o
treatment. Previous reports of patients stopping treatment in complete molecular; H9 I5 z+ Z4 G7 h4 E0 E
response have included only patients with a good response to imatinib. We, M' u v2 I+ l; N
describe three patients with stable complete molecular response on dasatinib
' W1 w% y& k+ u; y4 ctreatment following imatinib failure. Two of the three patients remain in
* B( a9 M$ `$ K( K4 ]complete molecular response more than 12 months after stopping dasatinib. In
! A6 f/ ?% Y, N4 j8 K) l( Uthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to' N- w% E0 K$ t0 R% K/ _: ]
show that the leukemic clone remains detectable, as we have previously shown in
; h( L' P4 }2 Rimatinib-treated patients. Dasatinib-associated immunological phenomena, such as' o3 `5 T: s& l5 I6 o2 y
the emergence of clonal T cell populations, were observed both in one patient1 Y4 {/ L# I) @. ]7 k% b6 m1 y
who relapsed and in one patient in remission. Our results suggest that the
/ ~' c' _( H" V$ W1 J/ m* C7 D# zcharacteristics of complete molecular response on dasatinib treatment may be
+ t j& \; l0 T/ J5 k$ Tsimilar to that achieved with imatinib, at least in patients with adverse
* E! U& B% G* ~: H- h: z gdisease features.9 p- C- T6 S4 x& Z
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