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1 inhibitors that are efficacious in cutaneous T cell lymphoma.
2 it is believed to be the cause of peripheral T cell lymphoma.
3 on of immature thymocytes and development of T cell lymphoma.
4 s with peripheral (PTCL) or cutaneous (CTCL) T-cell lymphoma.
5 es that demonstrated preliminary activity in T-cell lymphoma.
6 dy, in 41 pretreated patients with cutaneous T-cell lymphoma.
7 ggressive CD4+ leukemic variant of cutaneous T-cell lymphoma.
8 ymphoma, and four of eight with noncutaneous T-cell lymphoma.
9 drug approved for the treatment of cutaneous T-cell lymphoma.
10 se agents to treat skin cancer and cutaneous T-cell lymphoma.
11 ymphoma, Burkitt's lymphoma, or noncutaneous T-cell lymphoma.
12 pGs have demonstrated efficacy for cutaneous T-cell lymphoma.
13 h, including atopic dermatitis and cutaneous T-cell lymphoma.
14 ncer, lentigo maligna melanoma and cutaneous T-cell lymphoma.
15 AC inhibitors for the treatment of cutaneous T-cell lymphoma.
16 an attractive strategy for the treatment of T-cell lymphoma.
17 es the second most common group of cutaneous T-cell lymphoma.
18 nd management of relapsed angioimmunoblastic T-cell lymphoma.
19 dary suppression of p53 in invasive nasal NK/T-cell lymphoma.
20 cceptable toxicity in refractory or relapsed T-cell lymphoma.
21 n of 2 of 10 cases of enteropathy-associated T-cell lymphoma.
22 lymphoblastic T-cell leukemia and cutaneous T-cell lymphoma.
23 es (MF) is the most common primary cutaneous T-cell lymphoma.
24 ymphoma and large-cell transformed cutaneous T-cell lymphoma.
25 (MF) is the most frequent form of cutaneous T-cell lymphoma.
26 tory Hodgkin's lymphoma and anaplastic large-T-cell lymphoma.
27 sis fungoides, a common variant of cutaneous T-cell lymphoma.
28 activity in large-cell transformed cutaneous T-cell lymphoma.
29 could have a critical role in the biology of T-cell lymphoma.
30 a condensin II subunit (Caph2(nes)) develop T-cell lymphoma.
31 lating agent MNU, which predominantly caused T cell lymphomas.
32 ukemia (T-ALL) and in a subset of peripheral T-cell lymphomas.
33 icularly frequent in all forms of gammadelta-T-cell lymphomas.
34 3 expression developed colitis and alphabeta T-cell lymphomas.
35 ate safety and efficacy in CD30(+) cutaneous T-cell lymphomas.
36 and the role EBV plays in the development of T-cell lymphomas.
37 ne mechanism for the association of EBV with T-cell lymphomas.
38 lators that are required for the survival of T-cell lymphomas.
39 T-cell lymphoma and other primary cutaneous T-cell lymphomas.
40 indicating that Dnmt1 is required to sustain T-cell lymphomas.
41 BCL6 regulation and potential links to B and T-cell lymphomas.
42 cell leukemia/lymphoma, and other peripheral T-cell lymphomas.
43 reated patients with CD30-positive cutaneous T-cell lymphomas.
44 patients with relapsed or refractory B- and T-cell lymphomas.
45 gkin lymphomas and systemic anaplastic large T-cell lymphomas.
46 cell leukaemia-lymphoma and other peripheral T-cell lymphomas.
47 ne in mice gives rise to spontaneous thymic (T-cell) lymphomas.
48 egative (ALK[-]) ALCLs, 9 angioimmunoblastic T-cell lymphomas, 11 peripheral T-cell lymphomas not oth
49 lymphomas (6.3%) of which angioimmunoblastic T-cell lymphomas (2.3%) were the most frequent, and muco
50 lymphoma and one [2%] with anaplastic large-T-cell lymphoma; 28 [43%] during phase 1 and 37 [57%] du
51 classic Hodgkin lymphomas (13%), peripheral T-cell lymphomas (6.3%) of which angioimmunoblastic T-ce
52 ngioimmunoblastic T-cell lymphoma, cutaneous T-cell lymphoma, adult T-cell leukemia/lymphoma, and oth
54 present in 22 of 35 (67%) angioimmunoblastic T cell lymphoma (AITL) samples and in 8 of 44 (18%) PTCL
55 n 40 of 86 (47%) cases of angioimmunoblastic T-cell lymphoma (AITL) and in 22 of 58 (38%) cases of pe
60 L-entities, including 114 angioimmunoblastic T-cell lymphoma (AITL), 31 anaplastic lymphoma kinase (A
63 and a lower incidence of angioimmunoblastic T-cell lymphoma (AITL); Asians/Pacific Islanders had a h
64 Ls; n = 35), specifically angioimmunoblastic T-cell lymphoma (AITL; n = 13) and PTCL not otherwise sp
65 d (PTCL-NOS; n = 26) and angio-immunoblastic T-cell lymphoma (AITL; n = 46) patients treated with che
66 therwise specified [NOS], angioimmunoblastic T-cell lymphoma [AITL], and anaplastic large-cell lympho
68 on-Hodgkin, Hodgkin and nasal natural killer/T-cell lymphomas, although all three TET family genes ar
70 location was found in a subset of peripheral T cell lymphomas and was shown to result in an IL-2-indu
71 umor effect of rapamycin in a mouse model of T-cell lymphoma and examine the metabolic effects in vit
72 eneration proteasome inhibitor, ixazomib, in T-cell lymphoma and Hodgkin lymphoma cells and in vivo S
73 ibited tumor growth and improved survival in T-cell lymphoma and Hodgkin lymphoma human lymphoma xeno
75 gulates MYC and induces potent cell death in T-cell lymphoma and Hodgkin lymphoma, and we identified
76 t is approved for the treatment of cutaneous T-cell lymphoma and is used experimentally for the deple
77 lastic cells in primary cutaneous anaplastic T-cell lymphoma and large-cell transformed cutaneous T-c
79 ons in DNMT3A have been recently reported in T-cell lymphoma and leukemia, implying a possible involv
80 both active and well tolerated in cutaneous T-cell lymphoma and lymphomatoid papulosis, with an over
81 (MF) is the most common subtype of cutaneous T-cell lymphoma and may rarely infiltrate the ocular str
82 f AITL, extranodal nasal-type natural killer/T-cell lymphoma and NK-cell leukemia (ENKCL), and ATLL a
83 plastic transformation in angioimmunoblastic T-cell lymphoma and other primary cutaneous T-cell lymph
84 currently being used for treating cutaneous T-cell lymphoma and under clinical trials for multiple o
85 itical for the prevention and maintenance of T-cell lymphomas and contributes to aberrant methylation
86 oncogenic gammaherpesvirus that causes acute T-cell lymphomas and leukemias in New World primates and
89 logs are effective in treating leukemias and T cell lymphomas, and 6-ETI may fill this niche for the
90 acute lymphoblastic leukemia, natural killer/T-cell lymphoma, and acute myeloid leukemia, as well as
91 not otherwise specified, angioimmunoblastic T-cell lymphoma, and anaplastic lymphoma kinase (ALK)-ne
94 with relapsed or refractory B-cell lymphoma, T-cell lymphoma, and multiple myeloma received the anti-
95 mor immunity in primary cutaneous anaplastic T-cell lymphoma, and provide a rationale for the pharmac
96 ng classical Hodgkin lymphoma, T-cell and NK/T-cell lymphomas, and follicular dendritic cells neoplas
97 after chemotherapy for an angioimmunoblastic-T-cell-lymphoma, and thirty-three hours after being stru
100 n promotes genomic instability that leads to T-cell lymphomas as a consequence of altered double stra
101 s to compare in a large series of peripheral T cell lymphoma, as a model of diffuse disease, the prog
102 HTLV-1)-associated adult T-cell leukemia and T-cell lymphoma (ATL) are aggressive diseases with poor
103 roved for relapsed and refractory peripheral T-cell lymphomas based on their activity, although they
104 howing that ITK-Syk expression causes clonal T cell lymphoma by 20-27 wk of age, we investigated the
106 ested for their activity against L5178 mouse T-cell lymphoma cells (non-MDR) and their subcell line t
107 cycle arrest in primary cutaneous anaplastic T-cell lymphoma cells in vitro and a xenograft model in
108 yndrome is a rare leukemic form of cutaneous T cell lymphoma characterized by generalized redness, sc
109 s an incurable leukemic variant of cutaneous T-cell lymphoma characterized by recurrent chromosomal a
111 r early-stage nasal type natural killer (NK)/T-cell lymphoma, combined radiotherapy (RT), and chemoth
112 ) >/= 2; the Prognostic Index for Peripheral T-Cell Lymphoma, comprising: age >/= 60 years, PS >/= 2,
115 In this article, we report that cutaneous T cell lymphoma (CTCL) cells and tissues ubiquitously ex
117 a leukemic and aggressive form of cutaneous T cell lymphoma (CTCL) resulting from the malignant tran
118 hallmark of the advanced stages of cutaneous T cell lymphoma (CTCL), where it has been associated wit
120 rome (SS) is a leukemic variant of cutaneous T-cell lymphoma (CTCL) and represents an ideal model for
122 elomerase activity (TA) in primary cutaneous T-cell lymphoma (CTCL) by using quantitative polymerase
123 HDI) resistance, we selected HuT78 cutaneous T-cell lymphoma (CTCL) cells with romidepsin in the pres
124 ry syndrome are two major forms of cutaneous T-cell lymphoma (CTCL) characterized by resistance to ap
132 ell lymphoma line, MBL2, and human cutaneous T-cell lymphoma (CTCL) lines, HH and Hut78, were used in
134 ary syndrome (SS) is an aggressive cutaneous T-cell lymphoma (CTCL) of unknown etiology in which mali
135 blood involvement in patients with cutaneous T-cell lymphoma (CTCL) portend a worse clinical outcome.
137 red to six healthy control and six cutaneous T-cell lymphoma (CTCL) samples from previously published
138 nes established from patients with cutaneous T-cell lymphoma (CTCL) spontaneously secrete IL-17F and
139 as FDA approval as a treatment for cutaneous T-cell lymphoma (CTCL), although treatment with 1 can el
140 NA) dysregulation is a hallmark of cutaneous T-cell lymphoma (CTCL), an often-fatal malignancy of ski
141 fungoides, the most common type of cutaneous T-cell lymphoma (CTCL), as compared to normal skin or be
149 and for monitoring progression of cutaneous T-cell lymphoma (CTCL)/SS and that FCRL3 expression corr
150 1 is FDA-approved for treatment of cutaneous T-cell lymphoma (CTCL); however, 1 can provoke side effe
151 syndrome comprise the majority of cutaneous T cell lymphomas (CTCLs), disorders notable for their cl
156 diseases, the malignant T cells of cutaneous T-cell lymphomas (CTCLs), such as Sezary syndrome, displ
157 een shown to be hypermethylated in cutaneous T-cell lymphomas (CTCLs), using standard bisulfite modif
158 stic large-cell lymphoma, angioimmunoblastic T-cell lymphoma, cutaneous T-cell lymphoma, adult T-cell
159 nd (CEUS) findings in enteropathy associated T-cell lymphoma (EATL) complicating CMLNS in a gluten-fr
163 led the progression of OVA257-264 expressing T-cell lymphoma EG7 (injected intradermally), the deplet
164 linical outcome of extranodal natural killer T-cell lymphoma (ENKTL) has improved substantially as a
166 eous CD4+ small- to medium-sized pleomorphic T-cell lymphoma, especially in cases with a high percent
170 investigated the somatic mutations in B- and T-cell lymphomas from these breeds by exome sequencing o
172 s immune-mediated diseases such as cutaneous T cell lymphoma, graft-versus-host disease, and organ al
173 ctory Hodgkin's lymphoma or anaplastic large-T-cell lymphoma, had biopsy-proven CD30-positive tumours
177 V) is an alphaherpesvirus that causes deadly T-cell lymphomas in chickens and serves as a natural sma
182 e the levels of Rac1-GTP and the activity of T-cell lymphoma invasion and metastasis 1 (TIAM1), a Rac
183 rolled regulator of invasion and metastasis, T-cell lymphoma invasion and metastasis 1 (TIAM1), was i
185 lysis revealed that the Rac activator Tiam1 (T-cell lymphoma invasion and metastasis 1) is overexpres
186 thelial cell transforming squence 2), Tiam1 (T-cell lymphoma invasion and metastasis 1), Vav and P-Re
187 kinase activity results in the detachment of T-cell lymphoma invasion and metastasis-inducing protein
191 eous CD4+ small- to medium-sized pleomorphic T-cell lymphoma is listed as a provisional entity that i
193 acid is already approved to treat cutaneous T-cell lymphoma, it could potentially be used as a thera
194 T-cell lymphoma (n = 9), tMF (n = 7), adult T-cell lymphoma/leukemia (n = 4), anaplastic large-cell
197 found that Notch signaling represses Ccr9 in T cell lymphoma lines in which Ccr9 transcription is ind
198 ell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoma lines in vitro and significantly inhibit
199 of origin and lymphocyte ontogeny among the T-cell lymphomas may improve our understanding of the tu
200 ts with stage IA through stage IIA cutaneous T-cell lymphoma, MF type, to evaluate treatment using to
201 ma radiation (IR)-induced replication stress T-cell lymphoma mouse model, we observed a significant i
202 stage (stage IA through stage IIA) cutaneous T-cell lymphoma, mycosis fungoides (MF) type, resulted i
204 ded DLBCL (n = 21), MCL (n = 13), peripheral T-cell lymphoma (n = 8), transformed follicular lymphoma
205 rwise specified (n = 13), angioimmunoblastic T-cell lymphoma (n = 9), tMF (n = 7), adult T-cell lymph
206 sis (n = 9) and primary cutaneous anaplastic T-cell lymphomas (n = 2) responded; time to response was
207 5B in NK/T-cell lymphomas (n=51), gammadelta-T-cell lymphomas (n=43) and their cell lines (n=9) throu
208 tivating mutations of STAT3 and STAT5B in NK/T-cell lymphomas (n=51), gammadelta-T-cell lymphomas (n=
209 = 10; mycosis fungoides, n = 13; peripheral T-cell lymphoma, n = 5; other T-cell lymphomas, n = 5; m
210 13; peripheral T-cell lymphoma, n = 5; other T-cell lymphomas, n = 5; multiple myeloma, n = 27).
214 In the current study, using natural killer/T-cell lymphoma (NKTL) as a disease model, we found that
215 rexpressed in the majority of natural killer/T-cell lymphoma (NKTL), an aggressive lymphoid malignanc
217 aplastic large-cell lymphoma, 102 peripheral T-cell lymphoma not otherwise specified, 27 angioimmunob
218 mmunoblastic T-cell lymphomas, 11 peripheral T-cell lymphomas not otherwise specified (PTCLNOS), and
219 L) and in 22 of 58 (38%) cases of peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), but
223 L and NSCLC, as compared with other types of T-cell lymphoma or EGFR- and K-RAS-mutated NSCLC, respec
226 g pathway previously implicated in cutaneous T-cell lymphoma pathogenesis, JAK/STAT signaling, we use
227 in 252 nodal PTCL and enteropathy-associated T-cell lymphoma patients (excluding anaplastic lymphoma
230 ion in an elderly Asian man with undiagnosed T cell lymphoma presenting with fever of unknown origin,
231 c large cell lymphoma (ALCL) is a peripheral T-cell lymphoma presenting mostly in children and young
233 atment of immunodeficient mice bearing human T cell lymphomas promoted tumor cell apoptosis and tumor
234 c leukemia (CLL) and CD8-positive peripheral T cell lymphomas (PTCL) in EmuSRalpha-tTA;Teto-Cre;Dnmt3
253 ) represent a large proportion of peripheral T-cell lymphomas (PTCLs) with poorly understood pathogen
256 ial diagnosis among the commonest peripheral T-cell lymphomas (PTCLs; ie, PTCL not otherwise specifie
257 t analysis included patients with peripheral T-cell lymphomas (PTCLs; n = 35), specifically angioimmu
258 ukaemia-lymphoma, four with other peripheral T-cell lymphomas) receiving lenalidomide, dose-limiting
259 tically accelerated incidence of both B- and T-cell lymphomas relative to Emu-D1T286A or ATM-/- contr
260 are limited, and the genetic basis of these T cell lymphomas remains incompletely characterized.
262 randomly selected BCL6-positive human B- and T-cell lymphomas, revealed concurrent expression of BCL6
263 eity in chromosome instability-driven murine T-cell lymphoma samples, indicating ongoing chromosome i
264 utely transforming retrovirus AKT8 in rodent T-cell lymphoma/signal transducer and activator of trans
266 One hundred six patients with peripheral T cell lymphoma, staged with PET/CT, were enrolled from
267 frequent than CDKN2A (12%) in all cutaneous T-cell lymphoma stages using quantitative reverse transc
269 immunosuppression, whereas the hepatosplenic T-cell lymphoma subtype and cases with involvement of bo
270 the pathological and clinical aspects of the T-cell lymphoma subtypes as well as NK-cell lymphomas an
271 -cell leukaemia-lymphoma or other peripheral T-cell lymphoma subtypes, and at least one previous anti
272 n the NCI1312 phase 2 study of romidepsin in T-cell lymphoma suggested perturbation of the MAPK pathw
274 vitro and in vivo activity of everolimus in T-cell lymphoma (TCL) and pave the way for future combin
275 tudy investigated mTOR pathway activation in T-cell lymphoma (TCL) cell lines and assessed antitumor
276 NHL), chronic lymphocytic leukemia (CLL), or T-cell lymphoma (TCL) were treated with 25 or 75 mg duve
277 otein, the dominant form of ALK expressed in T cell lymphomas (TCLs), closely resembles cell activati
279 cell lymphoma (ALCL) is a distinct entity of T-cell lymphoma that can be divided into 2 subtypes base
280 astic large cell lymphoma (ALCL) is a mature T-cell lymphoma that can present as a systemic or primar
281 -cell leukemia/lymphoma and 44 extranodal NK/T-cell lymphoma that were further separated into NK-cell
282 cell lymphoma (ALCL), a specific subtype of T-cell lymphoma, the Rho family GTPases Cdc42 and Rac1 a
283 ients with Hodgkin's lymphoma and peripheral T-cell lymphoma, treatment with bendamustine alone only
284 onstrate that rapamycin suppresses growth of T-cell lymphoma tumors and leads to a reduction in aerob
286 t otherwise specified, 27 angioimmunoblastic T-cell lymphoma) undergoing autologous HCT (autoHCT; n =
287 es (MF) is the most common primary cutaneous T-cell lymphoma variant and is closely related to a rare
288 In 2 of 3 organ recipients, a cutaneous T-cell lymphoma was diagnosed 2 and 3 years after infect
289 ith a history of stage IV angioimmunoblastic T-cell lymphoma was diagnosed with osteomyelitis of the
292 f younger patients developing hepato-splenic T-cell lymphoma while taking thiopurines with and withou
293 psed or refractory systemic anaplastic large-T-cell lymphoma who previously received at least one che
294 eous CD4+ small- to medium-sized pleomorphic T-cell lymphoma with an admixture of numerous CD20+ B ce
295 cision confirmed relapsed angioimmunoblastic T-cell lymphoma with atypical lymphocytes expressing CD3
297 ALK was first identified in a subset of T-cell lymphomas with anaplastic large cell lymphoma (AL
298 AITL now resides under the umbrella of nodal T-cell lymphomas with follicular T helper phenotype.
299 hromatin accessibility profiles of cutaneous T cell lymphoma, with dynamic assessments of response an
300 ecause of an initial diagnosis of peripheral T-cell lymphoma, with little or no response, whereas the
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