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。) }/ Q4 O) Z9 L# N: 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。
+ P8 \! S$ r5 G9 l I' d3 D
$ X2 p+ w3 p; J9 O2 o/ t, h5 B- h作者:来自澳大利亚; i" o# Q. m- x5 H& e8 J
来源:Haematologica. 2011.8.9.
: G; y) M) U. S8 i# i- U- EDear Group,
# q& N8 t: s. V1 U0 L" \0 r0 o1 ]& F3 f7 v1 }; Y+ O% a, j
Some of you are on Dasatinib (Sprycel) and we wish to give news on all CML2 C1 o V! b* W! ~$ V- J
therapies. Here is a report from Australia on 3 patients who went off Sprycel: D& A8 m! Q( T; J
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients" }: `6 S, p3 B2 A1 S; B' y# G' R
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel
5 B1 M$ _" n9 W% }# Hdoes spike up the immune system so I hope more reports come out on this issue.& o+ g6 }3 w5 L2 z- C
5 Y, W6 a D4 R6 {: ]. Z0 \, a, y9 s% sThe remarkable news about Sprycel cessation is that all 3 patients had failed$ ^ d F ]) N
Gleevec and Sprycel was their second TKI so they had resistant disease. This is
# r5 j; ~% d. G: u! O. hdifferent from the stopping Gleevec trial in France which only targets patients
& V. ~; r" J6 ~' Pwho have done well on Gleevec.! \ N: C- X+ R9 g) T7 K
' Q) ?+ {: N8 A$ S
Hopefully, the doctors will report on a larger study and long-term to see if the
0 n! s8 O0 }, B* }% R- w0 O9 D# tresponse off Sprycel is sustained.0 c% ~& j7 W3 g7 N
+ _! w/ V- Q4 i% a
Best Wishes,; j# z+ O2 _ |6 u$ a
Anjana+ u. P) {; u6 I/ T9 `
/ ?. C) k* P2 E0 F; M
* Y! f! Y! k: j7 E, f
* a% a* L% l9 z% F: L4 {' p' WHaematologica. 2011 Aug 9. [Epub ahead of print]
- n; z8 T/ w6 [) eDurable complete molecular remission of chronic myeloid leukemia following$ ~% j. H3 |! F: x8 v
dasatinib cessation, despite adverse disease features.. h+ G( j- l* P. k, a- c
Ross DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.
2 {% e$ G w" p+ V5 l; qSource
* V! t4 D2 ]8 _7 I5 r* c9 hAdelaide, Australia;3 D/ l" L' Z& x9 F
6 E: ^9 r6 z3 z) I. U+ {. Q5 |Abstract9 {8 K) F6 ~# q5 h
Patients with chronic myeloid leukemia, treated with imatinib, who have a* K( p+ I$ u' `5 X L& c- l8 }1 x
durable complete molecular response might remain in CMR after stopping. h( V: q! l; j9 ?6 y6 m
treatment. Previous reports of patients stopping treatment in complete molecular
+ |' S' y3 Q$ ~9 Z9 t3 A- c5 t9 oresponse have included only patients with a good response to imatinib. We, Z* z1 F4 X+ h2 I2 @
describe three patients with stable complete molecular response on dasatinib- V7 f* L8 T) W% e" {
treatment following imatinib failure. Two of the three patients remain in, ^8 R7 O" l5 U5 O+ D( a5 F
complete molecular response more than 12 months after stopping dasatinib. In
! r) t3 j/ r4 i" H/ C7 P' D/ \; h% uthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
2 w( i* _+ l+ o, r; E0 Pshow that the leukemic clone remains detectable, as we have previously shown in3 V* Z( P7 B F1 p
imatinib-treated patients. Dasatinib-associated immunological phenomena, such as
+ E) }* z* R: F& J' Mthe emergence of clonal T cell populations, were observed both in one patient
3 V9 G- F$ R; w a, k8 f- Ewho relapsed and in one patient in remission. Our results suggest that the& W# I0 O0 _. {5 a' y# g; _# q
characteristics of complete molecular response on dasatinib treatment may be
8 D! ?5 m+ L9 v/ ?similar to that achieved with imatinib, at least in patients with adverse4 Q7 G4 h5 ~- t+ b
disease features.; y" ?2 S- h; b' R2 y
|