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1                                              ATLL is a severe malignancy with no effective treatment.
2                               We screened 36 ATLL patients and 24 ethnically matched controls and fou
3        CCR4 mutations were detected in 14/53 ATLL samples (26%) and consisted exclusively of nonsense
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
6 atory mechanisms in IL-2-dependent cells and ATLL patients.
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
10 cells, identified a novel connection between ATLL cells and tumor-resident regulatory T cells (Tregs)
11 of novel treatment agents, the prognosis for ATLL remains poor.
12  represent potential therapeutic targets for ATLL treatment.
13  PS-341 and Zol are effective treatments for ATLL and HHM, which are refractory to conventional thera
14 teins was also assessed in cultured or fresh ATLL cells.
15 clonal selection typically observed in human ATLL, which normally develops in 2 to 5% of individuals
16 exposed a tumor-suppressive role for PD-1 in ATLL.
17     NF-kappaB is constitutively activated in ATLL cells and is essential for leukemogenesis including
18 vation after receptor engagement by CCL22 in ATLL cells and conferred a growth advantage in long-term
19 sion seen in HTLV-1 infection, especially in ATLL.
20 ncoprotein Tax, which is rarely expressed in ATLL cells, has long been recognized for its involvement
21 osis, and down-regulated PTHrP expression in ATLL cells in vitro.
22 tantly, knockdown of PA28gamma expression in ATLL cells latently infected with HTLV-1 reactivates exp
23 ortant factors in the pathogenesis of HHM in ATLL and the expression of PTHrP can be activated by nuc
24 underscore the importance of this pathway in ATLL development and offer a therapeutic handle for this
25 ine zipper factor (HBZ) play a major role in ATLL development, by interfering with cellular functions
26  signaling pathway plays a prominent role in ATLL pathogenesis, mutational analysis of pathway compon
27 of genes and pathways that drive or initiate ATLL, but so far amenable drug targets have not been for
28  etiological agent of Adult T-cell Leukemia (ATLL).
29  agent of adult T-cell lymphocytic leukemia (ATLL), whereas HTLV-II has not been associated with hema
30 at of BIC in adult T-cell lymphoma/leukemia (ATLL) tumors.
31 )-associated adult T-cell leukemia lymphoma (ATLL) can be identified years before the clinical manife
32 is linked to adult T-cell leukemia lymphoma (ATLL).
33 ins from all adult T-cell leukemia-lymphoma (ATLL) cases and healthy carriers studied.
34 eukemia (1), adult T-cell leukemia/lymphoma (ATLL) (1), marginal zone leukemia (1), large granular ly
35 atients with adult T-cell leukemia/lymphoma (ATLL) (NCT02631746).
36 ymphoma, and adult T-cell leukemia/lymphoma (ATLL) and a lower incidence of angioimmunoblastic T-cell
37 cal agent of adult T cell leukemia/lymphoma (ATLL) and a number of lymphocyte-mediated inflammatory c
38 LV-1) causes adult T-cell leukemia/lymphoma (ATLL) and a variety of lymphoproliferative disorders.
39 ponsible for adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic
40 velopment of adult T-cell leukemia/lymphoma (ATLL) and the neuroinflammatory disease, HTLV-1-associat
41 the cause of adult T-cell leukemia/lymphoma (ATLL) and viral oncogenic proteins, Tax and Hbz, are cri
42 ns among the adult T-cell leukemia/lymphoma (ATLL) category have opposite biochemical activities, whi
43              Adult T cell leukemia/lymphoma (ATLL) is an aggressive malignancy caused by human T cell
44              Adult T-cell leukemia/lymphoma (ATLL) is an incurable disease where most patients succum
45 nificance of adult T-cell leukemia/lymphoma (ATLL) is still unclear.
46 ting disease adult T-cell leukemia/lymphoma (ATLL) or HTLV-associated myelopathy/tropical spastic par
47 nt cells and adult T-cell leukemia/lymphoma (ATLL) patient samples, however, Tax expression is very l
48 hat initiate adult T-cell leukemia/lymphoma (ATLL) remain unclear, in part from the lack of an animal
49 d in ex vivo adult T-cell leukemia/lymphoma (ATLL) samples, but not asymptomatic carriers.
50 irst case of adult T-cell leukemia/lymphoma (ATLL) that responded rapidly to combination therapy of b
51 virus causes adult T-cell leukemia/lymphoma (ATLL) that typically has a CD4(+) phenotype.
52           In adult T cell leukemia/lymphoma (ATLL), the FoxP3(+) population was distinct from the leu
53 atients with adult T-cell leukemia/lymphoma (ATLL), the viral transactivator does not appear to be ex
54 gic agent of adult T-cell leukemia/lymphoma (ATLL).
55 lasia termed adult T cell leukemia/lymphoma (ATLL).
56 gic agent of adult T-cell leukemia/lymphoma (ATLL).
57 cal agent of Adult T-cell Leukemia/Lymphoma (ATLL).
58 V-I) induces adult T cell leukemia/lymphoma (ATLL).
59 (10.4%), and adult T-cell leukemia/lymphoma (ATLL; 9.6%).
60              Adult T-cell /lymphomaleukemia (ATLL) is caused by human T-cell lymphotropic virus type
61                         Approximately 80% of ATLL patients develop humoral hypercalcemia of malignanc
62 s point, cytogenetic findings in 50 cases of ATLL were correlated with clinical characteristics.
63  zoledronic acid (Zol) on the development of ATLL and HHM using a novel bioluminescent mouse model.
64 icable to the main pathway of development of ATLL and that a multistep process of leukemogenesis is r
65 mogenesis is required for the development of ATLL.
66 mplicated by the range of natural history of ATLL, different recruitments of naive-to-therapy, refrac
67 ved in the remarkable genetic instability of ATLL cells.
68                         This animal model of ATLL will provide an important tool for the identificati
69 nction CCR4 mutations in the pathogenesis of ATLL and suggest that inhibition of CCR4 signaling might
70            To illuminate the pathogenesis of ATLL we performed whole transcriptome sequencing of puri
71 (+) cells may both retard the progression of ATLL and HTLV-1-associated inflammatory diseases and con
72  of p53 function after ionizing radiation of ATLL cells indicated an abnormal induction of the p53-re
73 be in part responsible for the resistance of ATLL cells to chemotherapy.
74 type, all indicators of clinical severity of ATLL.
75 2 and CD20 has been described in a subset of ATLL cases.
76 frequently in acute and lymphoma subtypes of ATLL.
77 molecular drivers and therapeutic targets of ATLL.
78 d whole transcriptome sequencing of purified ATLL patient samples and discovered recurrent somatic mu
79 ll lymphomas with characteristics similar to ATLL and elevated proliferation of infected human stem c
80 g this alarming outcome in nivolumab-treated ATLL may be broadly informative for the growing problem
81 shed HTLV-I-infected T-cell lines or ex vivo ATLL cell lysates.
82 appear to be aberrantly expressed in ex vivo ATLL cells nor in any of the established HTLV-I-infected
83  increased expression of Bcl-X(L) in ex vivo ATLL cells, especially from patients unresponsive to var
84 he p53 protein is stabilized also in ex vivo ATLL samples (10 of 10 studied) and that at least in 2 p
85  in infected T cells in vitro and in ex vivo ATLL samples.
86 ultured leukemic cells from 12 patients with ATLL by either DNA-binding assays, using DNA oligonucleo
87 aired, in ex vivo samples from patients with ATLL, in the absence of genetic mutations.
88 utologous leukemic clones from patients with ATLL.
89 icient (NOD/SCID) mice were xenografted with ATLL cells and treated with vehicle control, PS-341, Zol