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。# f4 \9 q) U$ C" `5 Y
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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0 Y8 l% L' M* Y/ G作者：来自澳大利亚6 J, A. B V7 z5 G& z" I
来源：Haematologica. 2011.8.9. G/ R( f, g' {- y6 x q7 n$ x: R% ~
Dear Group,
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Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML
7 n' D. b; |* R# \+ ^therapies. Here is a report from Australia on 3 patients who went off Sprycel
# _( t4 \* T2 R p5 k* T% Hafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients: r8 L4 p" s: C. n3 a: n
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
u/ Z5 r) I; o1 |: D/ m: ?' n, fdoes spike up the immune system so I hope more reports come out on this issue.4 t" l! ^* |! ~) v/ }
# ]- y* k7 Z0 M8 A2 ~- W0 NThe remarkable news about Sprycel cessation is that all 3 patients had failed( E2 t3 P5 }: C- y2 ~& ^
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
* l* B) b, h* ~9 m: X7 \different from the stopping Gleevec trial in France which only targets patients
- w7 c- M4 v! ^+ A4 {who have done well on Gleevec.! W n! _& w7 m- M! z1 }4 Y
' w( c' u) p# f' Z+ s5 N: uHopefully, the doctors will report on a larger study and long-term to see if the
8 S/ c$ ?: k# \+ T; Z& Jresponse off Sprycel is sustained.9 o& k% B: [3 U1 o
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Best Wishes,
/ g; j# s2 \! c4 J8 Q/ RAnjana
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Haematologica. 2011 Aug 9. [Epub ahead of print]2 \9 f! V F& X) \5 J
Durable complete molecular remission of chronic myeloid leukemia following
1 }- z5 l! R6 b; i/ A; n: tdasatinib cessation, despite adverse disease features.
" A9 F% N. _3 e* K/ O3 PRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.% y, Q" b; Z; N8 e W
Source% W8 z# ^/ k6 m [
Adelaide, Australia;
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) M# \. e) y- W- C0 r& K5 g" |Abstract8 x$ {8 ]% _% }# Q
Patients with chronic myeloid leukemia, treated with imatinib, who have a c5 C& u% D B& l, B7 N. l6 _
durable complete molecular response might remain in CMR after stopping
9 Z. W) ]9 A; K( T6 j3 E% @treatment. Previous reports of patients stopping treatment in complete molecular
7 ^) p( l8 ?4 ?) z5 `- uresponse have included only patients with a good response to imatinib. We) P5 X' I, _) ~
describe three patients with stable complete molecular response on dasatinib; s0 g4 \1 A9 {: j' U
treatment following imatinib failure. Two of the three patients remain in
1 B" E/ D% T5 A6 Q' S* W% Jcomplete molecular response more than 12 months after stopping dasatinib. In
4 G7 G0 j: c/ v, G8 tthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to0 U3 m/ S+ ]9 i
show that the leukemic clone remains detectable, as we have previously shown in- B' A3 A T5 F+ k$ z A5 P
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
! u8 L' v- c( b$ F' m1 fthe emergence of clonal T cell populations, were observed both in one patient4 Y2 e4 I/ w k
who relapsed and in one patient in remission. Our results suggest that the
9 m& Q3 H. a* a. \characteristics of complete molecular response on dasatinib treatment may be
" U" Y7 I5 M- E; v# esimilar to that achieved with imatinib, at least in patients with adverse; q' ?& ]" J/ w% e& j8 U# T. z
disease features.
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