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

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

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

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

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

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

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

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

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

32 antly angioimmunoblastic lymphadenopathy and PTCL not otherwise specified.

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

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

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

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

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

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

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

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

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

42 approach to the treatment of the most common PTCLs.

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

44 ients, 160 had histopathologically confirmed PTCL.

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

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

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

48 lymphoma cells within Vdelta1 TCR-expressing PTCL.

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

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

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

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

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

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

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

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

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

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

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

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

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

62 3/23) across all patients and 71% (10/14) in PTCL.

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

64 ncing to identify new genetic alterations in PTCL transformation.

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

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

67 ring alisertib with investigator's choice in PTCL.

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

69 iption factors are coordinately expressed in PTCL.

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

71 p53-associated tumor suppressor function in PTCL.

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

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

74 usion EFS24 stratifies subsequent outcome in PTCL.

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

76 diagnostic accuracy, and prognostication in PTCL.

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

78 characterizing clonal TCR rearrangements in PTCL.

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

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

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

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

83 inical practice to assess CD30 expression in PTCLs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 ional tool in the diagnostic workup of nodal PTCL.

141 7 European centers, 140 patients with nodal PTCL who underwent baseline PET/CT were selected.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 le for VAV1 signaling in the pathogenesis of PTCL.

158 rveillance mechanisms in the pathogenesis of PTCL.

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

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

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

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

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

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

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

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

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

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

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

170 ed ability to diagnose this uncommon type of PTCL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 cted in patients with relapsed or refractory PTCL.

190 as a single agent in relapsed or refractory PTCL.

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

192 antitumor activity in patients with relapsed PTCL particularly AITL.

193 durable responses in patients with relapsed PTCL.

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

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

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

197 3 family members MCL1 and BCL-XL sensitizing PTCL cells to BH3 mimetic drugs.

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

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

200 8 of 44 (18%) PTCL, not otherwise specified (PTCL-NOS) samples.

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

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

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

204 pective phase II study in untreated systemic PTCL.

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

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

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

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

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

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

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

212 The PTCLs are characterized by high remission rates after fr

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

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

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

216 ling, and outlines therapeutic approaches to PTCL.

217 nse rate in patients with previously treated PTCL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 e prognostic stratification of patients with PTCL.

235 gy in transplantation-eligible patients with PTCL.

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

237 ies to improve the outcome for patients with PTCL.

238 milar prognostic importance in patients with PTCL.

239 complete responses, all among patients with PTCL.

240 rge population-based cohort of patients with PTCL.

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