ライフサイエンスコーパス: PTCL

1 PTCL was not pathognomonic for any specific disease.

2 PTCL-C/C3 was found in acute (C, 20%; C3, 7%) and chroni

3 PTCL-C/C3 was rare in native kidneys (C, 6%; C3, 1%), as

4 PTCL-C3 was more predominant in cases with antibody-medi

5 PTCL-unclassifiable was molecularly heterogeneous, but w

6 PTCLs showed phenotypic features of activated NKT cells,

7 The vast majority of LEF-1+ and/or TCF-1+ PTCL (34 of 39 or 87%) exhibit a composite Th1 T-cell-li

8 repertoire of the neoplastic T-cells in 108 PTCL samples.

9 We studied 244 PTCLs, including 158 PTCLs NOS, 63 AITLs, and 23 ALK-negative ALCLs.

10 DNA libraries and applied these tools to 16 PTCL patient tissue samples and 6 PTCL cell lines.

11 lymphoma (AITL) samples and in 8 of 44 (18%) PTCL, not otherwise specified (PTCL-NOS) samples.

12 clinical relevance in a large cohort of 190 PTCL patients.

13 rearrangements were seen in 11 (5.8%) of 190 PTCLs and were associated with inferior overall survival

14 We studied 244 PTCLs, including 158 PTCLs NOS, 63 AITLs, and 23 ALK-neg

15 Gene-expression profiles on 372 PTCL cases were analyzed and robust molecular classifier

16 The 68 PTCLs include 45 PTCLs unspecified, 10 Ki-1 anaplastic (ALCL), 8 angioimm

17 ools to 16 PTCL patient tissue samples and 6 PTCL cell lines.

18 The 68 PTCLs include 45 PTCLs unspecified, 10 Ki-1 anaplastic (

19 Swedish Lymphoma Registry, we identified 755 PTCL patients diagnosed during a 10-year period.

20 t clones could be identified in 65 out of 76 PTCL cases (86%) with adequate TCR transcript expression

21 sociated malignancy in the context of t(5;9) PTCL.

22 ration of duvelisib to mice engrafted with a PTCL patient-derived xenograft resulted in a shift among

23 HDACi) as a class of drugs effective against PTCL-NOS(Smarcb1-).

24 late non-CH-associated mutations during AITL/PTCL-NOS development.

25 A subset of AITL/PTCL-NOS patients develop concomitant hematologic neopla

26 omic alterations, found in 70.4% of the AITL/PTCL-NOS patients, were shared among CH and T-cell lymph

27 ng demonstrated distinct clustering of ALCL, PTCL-NOS, and the AITL subtype of PTCL.

28 In allografts, PTCL-C/C3 was significantly more common, especially in s

29 Among PTCL-NOS, a heterogeneous group of lymphoma-comprising c

30 noblastic T-cell lymphoma (AITL; n = 13) and PTCL not otherwise specified (n = 22).

31 s were identified (ALCL, 35%; AITL, 21%; and PTCL NOS, 44%).

32 In the AITL and PTCL-NOS subgroups, TET2 mutations were associated with

33 ficantly over-expressed in cases of AITL and PTCL-NOS that had favorable outcomes.

34 d the proliferation of malignant T cells and PTCL progression in these models.

35 serve as a new mouse model to study CLL and PTCL in relevant physiological settings.

36 ecular comparison of mouse and human CLL and PTCL reveals significant overlaps and identifies putativ

37 difference in OS between the PTCL-GATA3 and PTCL-TBX21 subtypes was confirmed (P = .003).

38 lecular subtypes of PTCL-NOS, PTCL-GATA3 and PTCL-TBX21, which have distinct biological differences i

39 eviously unsuspected link between Lin28b and PTCL, and provide a unique animal model for the study of

40 antly angioimmunoblastic lymphadenopathy and PTCL not otherwise specified.

41 Annual PTCL incidence was highest in blacks and lowest in Nativ

42 imately one-third of cases are designated as PTCL-not otherwise specified (PTCL-NOS).

43 ymphomas [TCRBCLs] have been misdiagnosed as PTCLs in the past) and because its correlation with othe

44 This study is the largest population-based PTCL cohort reported so far and provides important infor

45 ypes of PTCL and the prognostication of both PTCL-not otherwise specified (PTCL-NOS; n = 26) and angi

46 ront-line treatment in patients with CD30(+) PTCL.

47 ity in newly diagnosed patients with CD30(+) PTCL.

48 y of BV-CHP in less common subtypes of CD30+ PTCL subtypes await clarification.

49 CL from PTCL NOS, especially from some CD30+ PTCL NOS with uncertain morphology.

50 are practice changing for common nodal CD30+ PTCLs.

51 ntly 50% of PTCL cases are not classifiable: PTCL-not otherwise specified (NOS).

52 The most common PTCLs, peripheral T-cell lymphoma, not otherwise specifi

53 approach to the treatment of the most common PTCLs.

54 s enrolled, 130 had histologically confirmed PTCL by central review.

55 ients, 160 had histopathologically confirmed PTCL.

56 ents with AITL (n = 72) or other TFH-derived PTCL (n = 13) by targeted deep sequencing of a gene pane

57 y-seven percent of morphologically diagnosed PTCL-NOS cases were reclassified into other specific sub

58 hal peripheral T cell lymphoma-like disease (PTCL), named malignant catarrhal fever (MCF).

59 al, separating high from low CD30-expressing PTCL cases.

60 lymphoma cells within Vdelta1 TCR-expressing PTCL.

61 For PTCL-NOS and AITL, we obtained 2 distinct prognostic sig

62 Highest odds ratios (81-117) for PTCL-C/C3 were noted in combined injuries, that is, mixe

63 than 2 (poor prognosis), the 5-year FFS for PTCL and BCLCL is 11% and 35%, respectively (P = .044),

64 ater than 2 (poor prognosis), 5-year FFS for PTCL and BCLCL is 26% and 38%, respectively (P = .03), a

65 than 3 (good prognosis), the 5-year FFS for PTCL and BCLCL is 49% and 64%, respectively (P = .001),

66 than 3 (good prognosis), the 5-year FFS for PTCL and BCLCL is 56% and 69%, respectively (P = .01), a

67 a diagnostic and prognostic significance for PTCL, offering new tools for patient care and follow-up.

68 improves and as treatments specifically for PTCL are developed, risk stratification has become a mor

69 strategies for optimizing immune therapy for PTCL are currently under investigation and have the pote

70 e of AHCT as early consolidation therapy for PTCL patients who are chemosensitive after induction che

71 The 5-year failure-free survival (FFS) for PTCLs and B-cell large-cell lymphomas (BCLCLs) is 38% an

72 ating either AITL and ALK-negative ALCL from PTCL NOS in a training set.

73 ed the distinction of ALK-negative ALCL from PTCL NOS, especially from some CD30+ PTCL NOS with uncer

74 sion profiles (GEPs; index test) to identify PTCL subtype.

75 nest peripheral T-cell lymphomas (PTCLs; ie, PTCL not otherwise specified [NOS], angioimmunoblastic T

76 3/23) across all patients and 71% (10/14) in PTCL.

77 cytidine and romidepsin are highly active in PTCL patients and could serve as a platform for novel re

78 epigenetic modifiers are potently active in PTCL patients.

79 Alisertib has antitumor activity in PTCL, including heavily pretreated patients.

80 ncing to identify new genetic alterations in PTCL transformation.

81 tologous stem-cell transplantation (ASCT) in PTCL, the Nordic Lymphoma Group (NLG) conducted a large

82 smal outcome of conventional chemotherapy in PTCL patients, these data suggest the hypothesis that th

83 ring alisertib with investigator's choice in PTCL.

84 pathway is highly vulnerable to THZ1 even in PTCL cells that carry the activating STAT3 mutation Y640

85 iption factors are coordinately expressed in PTCL.

86 ddition, LIN28B is overexpressed 7.5-fold in PTCL patient samples compared with activated CD4(+) cell

87 p53-associated tumor suppressor function in PTCL.

88 provides important information on outcome in PTCL outside the setting of clinical trials.

89 s not associated with an improved outcome in PTCL-NOS or angioimmunoblastic type, but was associated

90 usion EFS24 stratifies subsequent outcome in PTCL.

91 ion of genes in the TCR signaling pathway in PTCL, a common feature of chronically activated T cells.

92 diagnostic accuracy, and prognostication in PTCL.

93 As TP53 mutations are rare in PTCL compared with other malignancies, our findings sugg

94 characterizing clonal TCR rearrangements in PTCL.

95 e present study indicate that CNS relapse in PTCL occurs at a frequency similar to what is seen in ag

96 igands (DLL1/DLL4) play a pathogenic role in PTCL.

97 (VAV1-THAP4, VAV1-MYO1F, and VAV1-S100A7) in PTCL.

98 ng, study design, and risk stratification in PTCL.

99 A phase 2 study in PTCL will determine the efficacy of the combination.

100 inical practice to assess CD30 expression in PTCLs.

101 Activating NKRs were functional in PTCLs and dependent on SYK activity.

102 s, the histologic subtypes enrolled included PTCL not otherwise specified (n = 13), angioimmunoblasti

103 ents with PTCL of various subtypes including PTCL NOS, angioimmunoblastic, ALK-negative anaplastic la

104 ions made by the collaborative International PTCL Project, discusses prognostic issues and gene expre

105 Of the Th1-like PTCL studied, 33 of 42 (79%) were immunoreactive for LEF

106 rprisingly, none of the 21 cases of Th2-like PTCL studied, all cases of anaplastic large cell lymphom

107 ssion may be lost in Th2 T cells or Th2-like PTCL.

108 Peripheral T-cell lymphoma (PTCL) and natural killer/T-cell lymphoma (NKTCL) are rar

109 to an aggressive peripheral T-cell lymphoma (PTCL) characterized by widespread infiltration of parenc

110 er patients with peripheral T-cell lymphoma (PTCL) consolidated with autologous or allogeneic transpl

111 Peripheral T-cell lymphoma (PTCL) encompasses a heterogeneous group of neoplasms wit

112 eral subtypes of peripheral T-cell lymphoma (PTCL) in first remission.

113 Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of aggressive non-Hodgkin

114 Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of mature T-cell malignan

115 Peripheral T-cell lymphoma (PTCL) is a poor prognosis subtype of non-Hodgkin's lymph

116 Peripheral T-cell lymphoma (PTCL) is a rare, heterogeneous type of non-Hodgkin lymph

117 Peripheral T-cell lymphoma (PTCL) is often challenging to diagnose and classify.

118 ell clonality of peripheral T-cell lymphoma (PTCL) is routinely evaluated with a PCR-based method usi

119 veloped model of peripheral T cell lymphoma (PTCL) using the ITK-SYK fusion gene should serve as a po

120 bset of cases of peripheral T cell lymphoma (PTCL), 39 of 81 cases (48%), are immunoreactive for LEF-

121 or patients with peripheral T-cell lymphoma (PTCL), outcomes using frontline treatment with cyclophos

122 apsed/refractory peripheral T-cell lymphoma (PTCL).

123 bowel disease or peripheral T-cell lymphoma (PTCL).

124 ed or refractory peripheral T-cell lymphoma (PTCL).

125 etter understand peripheral T-cell lymphoma (PTCL).

126 in patients with peripheral T-cell lymphoma (PTCL).

127 ubtype of mature peripheral T-cell lymphoma (PTCL).

128 bout the risk in peripheral T-cell lymphoma (PTCL).

129 MCL; n = 7), and peripheral T-cell lymphoma (PTCL; n = 5).

130 tory peripheral T-cell non-Hodgkin lymphoma (PTCL).

131 Peripheral T-cell lymphomas (PTCL) are a group of rare malignancies characterized by

132 The peripheral T-cell lymphomas (PTCL) are a heterogeneous group of non-Hodgkin's lymphom

133 Peripheral T-cell lymphomas (PTCL) are aggressive diseases with poor response to chem

134 nd CD8-positive peripheral T cell lymphomas (PTCL) in EmuSRalpha-tTA;Teto-Cre;Dnmt3a(fl/fl); Rosa26LO

135 ne treatment of peripheral T-cell lymphomas (PTCL) involves regimens such as cyclophosphamide, doxoru

136 Peripheral T cell lymphomas (PTCLs) are a heterogeneous and poorly understood group o

137 Peripheral T cell lymphomas (PTCLs) are a heterogeneous entity of neoplasms with poor

138 Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of clinically aggressiv

139 Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of non-Hodgkin lymphoma

140 Peripheral T cell lymphomas (PTCLs) are a heterogeneous group of orphan neoplasms.

141 Peripheral T-cell lymphomas (PTCLs) are aggressive malignancies of mature T lymphocyt

142 Peripheral T cell lymphomas (PTCLs) are heterogeneous neoplasms and represent about 1

143 Peripheral T-cell lymphomas (PTCLs) are rare lymphomas with mostly poor outcome with

144 The peripheral T-cell lymphomas (PTCLs) are uniquely sensitive to epigenetic modifiers.

145 The peripheral T-cell lymphomas (PTCLs) encompass a heterogeneous group of diseases that

146 Purpose Peripheral T-cell lymphomas (PTCLs) have aggressive clinical behavior.

147 Peripheral T-cell lymphomas (PTCLs) represent a diverse group of non-Hodgkin lymphoma

148 Systemic peripheral T-cell lymphomas (PTCLs) respond poorly to conventional therapy.

149 e proportion of peripheral T-cell lymphomas (PTCLs) with poorly understood pathogenesis and unfavorab

150 ) nonanaplastic peripheral T-cell lymphomas (PTCLs) with promising efficacy.

151 g patients with peripheral T cell lymphomas (PTCLs), overall and complete response rates of duvelisib

152 the most common peripheral T-cell lymphomas (PTCLs).

153 ore recently in peripheral T-cell lymphomas (PTCLs).

154 e management of peripheral T-cell lymphomas (PTCLs).

155 g the commonest peripheral T-cell lymphomas (PTCLs; ie, PTCL not otherwise specified [NOS], angioimmu

156 d patients with peripheral T-cell lymphomas (PTCLs; n = 35), specifically angioimmunoblastic T-cell l

157 r peripheral T-cell non-Hodgkin's lymphomas (PTCLs) has been inconsistently reported in part because

158 relapsed or refractory PTCL across all major PTCL subtypes, regardless of the number or type of prior

159 r microenvironment were identified for major PTCL-entities, including 114 angioimmunoblastic T-cell l

160 ging high response rate across the two major PTCL subtypes, independent of age and prior treatment, w

161 hat p53-deficient mice also developed mature PTCLs that did not originate from conventional T cells b

162 capillary basement membrane multilamination (PTCL) is a hallmark of antibody-mediated chronic renal a

163 verall survival (OS) in large, multinational PTCL cohorts.

164 Human and murine PTCL-NOS(SMARCB1-) show similar DNA methylation profiles

165 PTCL ex vivo culture and in two STAT3-mutant PTCL xenografts, delineating a potential targeted agent-

166 DNMT3A-mutated PTCL-TBX21 cases showed inferior overall survival (OS),

167 an intention-to-treat analysis in 252 nodal PTCL and enteropathy-associated T-cell lymphoma patients

168 ional tool in the diagnostic workup of nodal PTCL.

169 7 European centers, 140 patients with nodal PTCL who underwent baseline PET/CT were selected.

170 cal characteristics of the most common nodal PTCLs by focusing on the contribution given by high-thro

171 microarrays in a cohort of 376 noncutaneous PTCLs representative of the main entities.

172 ined 2 major molecular subtypes of PTCL-NOS, PTCL-GATA3 and PTCL-TBX21, which have distinct biologica

173 tected disease in only 67% of MZL and 40% of PTCL.

174 Currently 50% of PTCL cases are not classifiable: PTCL-not otherwise spec

175 Conversely, the absence of PTCL-C3 is helpful in excluding chronic, Banff category

176 sion profiling was performed on 144 cases of PTCL and natural killer cell lymphoma and robust molecul

177 A cohort of 1,314 cases of PTCL and NKTCL was organized from 22 centers worldwide,

178 ical and pathologic features of 340 cases of PTCL, not otherwise specified.

179 In a training cohort of 49 cases of PTCL-NOS with corresponding GEP data, the 2 subtypes ide

180 In a large cohort of PTCL-NOS biopsies, Notch1 activation was significantly a

181 y reported in part because the definition of PTCL has been imprecise (eg, T-cell-rich B-cell non-Hodg

182 A diagnosis of PTCL or NKTCL was confirmed in 1,153 (87.8%) of the case

183 he biology underpinning the heterogeneity of PTCL improves and as treatments specifically for PTCL ar

184 nic whites, blacks had a higher incidence of PTCL not otherwise specified (PTCL-NOS), anaplastic larg

185 nd Native Americans had a lower incidence of PTCL-NOS (all P < .05).

186 L, and lends support to a bipartite model of PTCL development, based on expression of activation mark

187 Based on synergy in preclinical models of PTCL, we initiated a phase 1 study of pralatrexate plus

188 f the genetics and molecular pathogenesis of PTCL, with a resulting paucity of molecular targets for

189 rveillance mechanisms in the pathogenesis of PTCL.

190 le for VAV1 signaling in the pathogenesis of PTCL.

191 The presence of PTCL-C3 is a helpful adjunct finding to diagnose rejecti

192 nal landscape and transcriptomic profiles of PTCL entities, defined the cell of origin as a major det

193 ad efforts focused on molecular profiling of PTCL, NOS is likely to identify distinct subtypes that w

194 iking variation in incidence, proportions of PTCL subtypes, and survival was observed.

195 We analyzed the diagnostic significance of PTCL and propose diagnostic strategies.

196 ovide a unique animal model for the study of PTCL biology and therapy.

197 on, GATA-3 expression identified a subset of PTCL, NOS with distinct clinical features, including inf

198 These results define a new subtype of PTCL and pave the way for the development of blocking an

199 g of ALCL, PTCL-NOS, and the AITL subtype of PTCL.

200 ification is useful for defining subtypes of PTCL and NKTCL.

201 ul in both the diagnosis of some subtypes of PTCL and the prognostication of both PTCL-not otherwise

202 and pathologic features of rare subtypes of PTCL including EATL/MEITL, SPTCL, and HSTCL.

203 g can serve to identify specific subtypes of PTCL, and lends support to a bipartite model of PTCL dev

204 iously defined 2 major molecular subtypes of PTCL-NOS, PTCL-GATA3 and PTCL-TBX21, which have distinct

205 bing outcomes in the most common subtypes of PTCL: PTCL not otherwise specified, nodal T-follicular h

206 rrently an exciting time in the treatment of PTCL due to the advent of recently approved drugs as wel

207 ed ability to diagnose this uncommon type of PTCL.

208 However, the predictive diagnostic value of PTCL is incompletely studied.

209 Positive predictive values of PTCL-C and C3 are the following: all rejection types, 89

210 GATA-3 expression was observed in 45% of PTCLs, not otherwise specified (PTCL, NOS) and was assoc

211 , providing further evidence that a group of PTCLs NOS shares a Tfh derivation with but is distinct f

212 nced lymphoid malignancies, with emphasis on PTCL.

213 Studies that focus specifically on PTCL are emerging, with the ultimate goal of improved un

214 In several prospective trials, only PTCL patients with responsive disease after induction ch

215 ears with advanced-stage ALK- ALCL, AITL, or PTCL, the use of ASCT consolidation, but not the additio

216 ied (PTCL-NOS), but were absent in all other PTCL entities, with the exception of 2 of 10 cases of en

217 naplastic large-cell lymphomas, 57% of other PTCL entities were CD30-positive at a 5% threshold.

218 ) that differentiates ALK(-) ALCL from other PTCLs.

219 stic large cell lymphoma (n = 32) from other PTCLs.

220 limited number of Native American patients, PTCL subtype frequencies in this group were distinct but

221 onducted in cutaneous (CTCL) and peripheral (PTCL) T-cell lymphoma.

222 sing candidate for patients with peripheral (PTCL) or cutaneous (CTCL) T-cell lymphoma.

223 ng agents that we established in preclinical PTCL models, we conducted a phase 1 study of oral 5-azac

224 mproves lymphoma growth control in a primary PTCL ex vivo culture and in two STAT3-mutant PTCL xenogr

225 utcomes in the most common subtypes of PTCL: PTCL not otherwise specified, nodal T-follicular helper

226 mong patients with relapsed/refractory (R/R) PTCL.

227 isib in patients with relapsed or refractory PTCL (n = 16) and CTCL (n = 19), along with in vitro and

228 city in patients with relapsed or refractory PTCL across all major PTCL subtypes, regardless of the n

229 city in patients with relapsed or refractory PTCL across the major subtypes, irrespective of number o

230 durable responses in relapsed or refractory PTCL irrespective of age, histologic subtypes, amount of

231 cted in patients with relapsed or refractory PTCL.

232 as a single agent in relapsed or refractory PTCL.

233 ration for patients with relapsed/refractory PTCL, exhibiting response rates of 25% and 29% respectiv

234 t-eligible patients with relapsed/refractory PTCL.

235 antitumor activity in patients with relapsed PTCL particularly AITL.

236 durable responses in patients with relapsed PTCL.

237 subgroups can be identified in the remaining PTCL-NOS cases characterized by high expression of eithe

238 a poor survival compared with the remaining PTCL-not otherwise specified cases.

239 come and allows early detection of high-risk PTCL patients.

240 g pathologists and was validated in a second PTCL-NOS cohort (n = 124), where a significant differenc

241 3 family members MCL1 and BCL-XL sensitizing PTCL cells to BH3 mimetic drugs.

242 ron microscopy (terminology: PTCL-C, severe; PTCL subgroup C3, very severe multilamination; see Mater

243 ed in 45% of PTCLs, not otherwise specified (PTCL, NOS) and was associated with distinct molecular fe

244 8 of 44 (18%) PTCL, not otherwise specified (PTCL-NOS) samples.

245 r incidence of PTCL not otherwise specified (PTCL-NOS), anaplastic large-cell lymphoma, and adult T-c

246 al T-cell lymphoma, not otherwise specified (PTCL-NOS), but were absent in all other PTCL entities, w

247 al T-cell lymphoma, not otherwise specified (PTCL-NOS), remain poorly understood.

248 designated as PTCL-not otherwise specified (PTCL-NOS).

249 cation of both PTCL-not otherwise specified (PTCL-NOS; n = 26) and angio-immunoblastic T-cell lymphom

250 ally engineered mouse models and spontaneous PTCL models were used to functionally examine the role o

251 Here, we identify a subgroup, PTCL-NOS(SMARCB1-), which is characterized by the lack o

252 pective phase II study in untreated systemic PTCL.

253 Patients and Methods Patients with systemic PTCL newly diagnosed from 2000 to 2012 and treated with

254 tification of effective strategies to target PTCL biology represents an urgent need.

255 ecimens by electron microscopy (terminology: PTCL-C, severe; PTCL subgroup C3, very severe multilamin

256 discriminated some T-follicular helper (Tfh) PTCL NOS from AITL, providing further evidence that a gr

257 ation, three times more frequent in CLL than PTCL and correlated better with gene expression than hyp

258 Here we report that PTCL are sensitive to transcription-targeting drugs, and

259 CBR among the PTCL cases (n = 45) in cohorts 1, 2, and 3 were 53%, 45%

260 Among the PTCL subtypes, the overall response rate was 30%, wherea

261 ational Prognostic Index score (3-5) and the PTCL-GATA3 subtype identified by IHC were independent ad

262 e a significant difference in OS between the PTCL-GATA3 and PTCL-TBX21 subtypes was confirmed (P = .0

263 an activated CD8+ cytotoxic phenotype in the PTCL-TBX21 subtype (P = .03).

264 The PTCLs are characterized by high remission rates after fr

265 The PTCLs that develop in Lin28b mice are derived from activ

266 Aspects of these PTCL subtype patterns, such as for ENKCL and ATLL, were

267 NKT cells, increased the incidence of these PTCLs, whereas Escherichia coli injection did not.

268 ling, and outlines therapeutic approaches to PTCL.

269 ummary of ongoing clinical trials related to PTCL is presented, with the aim of aiding clinicians in

270 nse rate in patients with previously treated PTCL.

271 isting of patients with previously untreated PTCL or NKTCL who were diagnosed between 1990 and 2002.

272 ession and granulocyte activation in various PTCL mouse models.

273 The most common subtypes were PTCL not otherwise specified (NOS; 25.9%), angioimmunobl

274 f a total of 560 evaluable patients, 68 were PTCLs (12%) and the remaining 492 (88%) were B-cell non-

275 AITL, TET2 mutations were more frequent when PTCL-NOS expressed T(FH) markers and/or had features rem

276 ymphomagenesis and cell-of-origin from which PTCLs arise is crucial for the development of efficient

277 Patients with PTCL (age >/= 15 years; 2000 to 2012) were identified in

278 Treatment-naive patients with PTCL age 18 to 67 years (median, 57 years) were included

279 The overall response rates in patients with PTCL and CTCL were 50.0% and 31.6%, respectively (P = .3

280 patients despite the fact that patients with PTCL are known to have a worse outcome compared with B-c

281 Forty-seven patients with PTCL of various subtypes including PTCL NOS, angioimmuno

282 owever, more than one third of patients with PTCL remain in remission 2 years after diagnosis with en

283 s substantially more active in patients with PTCL than in those with non-T-cell lymphoma.

284 present study, a cohort of 122 patients with PTCL was collected from a multicentric T-cell lymphoma c

285 een thousand one hundred seven patients with PTCL were identified.

286 ELON-2, frontline treatment of patients with PTCL with A+CHP continues to provide clinically meaningf

287 Patients with PTCL with primary refractory disease or early relapse ha

288 Similar to patients with PTCL, Lin28b-transgenic mice show signs of inflammation

289 ture could be used to stratify patients with PTCL-not otherwise specified for novel and risk-adapted

290 e prognostic stratification of patients with PTCL.

291 gy in transplantation-eligible patients with PTCL.

292 PFS in 44% of treatment-naive patients with PTCL.

293 ies to improve the outcome for patients with PTCL.

294 milar prognostic importance in patients with PTCL.

295 complete responses, all among patients with PTCL.

296 rge population-based cohort of patients with PTCL.

297 ty-eight patients (48 men and 30 women) with PTCL seen at a single institution between 1985 and 1995

298 e progression-free survival of patients with PTCLs needs to be improved.

299 cells, the overall survival of patients with PTCLs will dramatically increase.

300 analysis of DNMT3A-mutant vs wild-type (WT) PTCL-TBX21 cases demonstrated hypomethylation in target