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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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