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1 ATLL is a severe malignancy with no effective treatment.
4 motherapy regimens and mAbs directed against ATLL tumor markers do not alter this aggressive clinical
5 sed in both untransformed infected cells and ATLL cells and is involved in sustaining cell proliferat
7 PTCL subtype patterns, such as for ENKCL and ATLL, were similar to corresponding global populations.
8 l lymphoma and NK-cell leukemia (ENKCL), and ATLL and a lower incidence of anaplastic large-cell lymp
9 c paraparesis-HTLV-associated myelopathy and ATLL or healthy carriers may be relevant in vivo, since
12 PS-341 and Zol are effective treatments for ATLL and HHM, which are refractory to conventional thera
14 NF-kappaB is constitutively activated in ATLL cells and is essential for leukemogenesis including
15 vation after receptor engagement by CCL22 in ATLL cells and conferred a growth advantage in long-term
17 ncoprotein Tax, which is rarely expressed in ATLL cells, has long been recognized for its involvement
19 tantly, knockdown of PA28gamma expression in ATLL cells latently infected with HTLV-1 reactivates exp
20 ortant factors in the pathogenesis of HHM in ATLL and the expression of PTHrP can be activated by nuc
21 underscore the importance of this pathway in ATLL development and offer a therapeutic handle for this
22 ine zipper factor (HBZ) play a major role in ATLL development, by interfering with cellular functions
23 signaling pathway plays a prominent role in ATLL pathogenesis, mutational analysis of pathway compon
24 of genes and pathways that drive or initiate ATLL, but so far amenable drug targets have not been for
26 agent of adult T-cell lymphocytic leukemia (ATLL), whereas HTLV-II has not been associated with hema
30 eukemia (1), adult T-cell leukemia/lymphoma (ATLL) (1), marginal zone leukemia (1), large granular ly
31 ymphoma, and adult T-cell leukemia/lymphoma (ATLL) and a lower incidence of angioimmunoblastic T-cell
32 LV-1) causes adult T-cell leukemia/lymphoma (ATLL) and a variety of lymphoproliferative disorders.
33 ns among the adult T-cell leukemia/lymphoma (ATLL) category have opposite biochemical activities, whi
37 nt cells and adult T-cell leukemia/lymphoma (ATLL) patient samples, however, Tax expression is very l
38 hat initiate adult T-cell leukemia/lymphoma (ATLL) remain unclear, in part from the lack of an animal
40 irst case of adult T-cell leukemia/lymphoma (ATLL) that responded rapidly to combination therapy of b
43 atients with adult T-cell leukemia/lymphoma (ATLL), the viral transactivator does not appear to be ex
53 zoledronic acid (Zol) on the development of ATLL and HHM using a novel bioluminescent mouse model.
54 icable to the main pathway of development of ATLL and that a multistep process of leukemogenesis is r
56 mplicated by the range of natural history of ATLL, different recruitments of naive-to-therapy, refrac
59 nction CCR4 mutations in the pathogenesis of ATLL and suggest that inhibition of CCR4 signaling might
61 (+) cells may both retard the progression of ATLL and HTLV-1-associated inflammatory diseases and con
62 of p53 function after ionizing radiation of ATLL cells indicated an abnormal induction of the p53-re
66 d whole transcriptome sequencing of purified ATLL patient samples and discovered recurrent somatic mu
67 ll lymphomas with characteristics similar to ATLL and elevated proliferation of infected human stem c
69 appear to be aberrantly expressed in ex vivo ATLL cells nor in any of the established HTLV-I-infected
70 increased expression of Bcl-X(L) in ex vivo ATLL cells, especially from patients unresponsive to var
71 he p53 protein is stabilized also in ex vivo ATLL samples (10 of 10 studied) and that at least in 2 p
73 ultured leukemic cells from 12 patients with ATLL by either DNA-binding assays, using DNA oligonucleo
76 icient (NOD/SCID) mice were xenografted with ATLL cells and treated with vehicle control, PS-341, Zol
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