ライフサイエンスコーパス: ALCL

1 ALCL cells that were deficient in ARNT exhibited defects

2 ALCL is defined by the presence or absence of translocat

3 95L/FASL was expressed in only 3 (12%) of 26 ALCL tumors, although it was strongly expressed by surro

4 uate the growth and proliferation of ALK (+) ALCL cells.

5 alogues were also highly expressed in ALK(+) ALCL and may represent important downstream effectors of

6 as a potential therapeutic target in ALK(+) ALCL and possibly other types of malignant lymphoma.

7 -IR and IGF-I are widely expressed in ALK(+) ALCL cell lines and primary tumors.

8 ssion of Th17-associated molecules in ALK(+) ALCL was noted and may represent aberrant activation of

9 explored a possible role of IGF-IR in ALK(+) ALCL.

10 itive anaplastic large-cell lymphoma (ALK(+) ALCL) is a unique type of T-cell lymphoma.

11 cJun phosphorylation in NPM-ALK(+) ALCL cells is mediated by JNKs, as shown by selective kn

12 ly, inhibition of ALK activity in NPM-ALK(+) ALCL cells resulted in a concentration-dependent dephosp

13 activated in cultured and primary NPM-ALK(+) ALCL cells.

14 Cases of ALK(+) ALCL and ALK(-) ALCL were interspersed in unsupervised a

15 Approximately 85% of ALK(+) ALCL cases harbor the translocation t(2;5)(p23;q35), whi

16 proliferation and colony formation of ALK(+) ALCL cell lines.

17 iR-155) significantly associated with ALK(+) ALCL cases.

18 -positive (ALK(+)) lymphomas and human ALK(+)ALCL cell lines, in the present study, we show that high

19 -1 and IL-8 receptors are expressed in ALK(+)ALCL biopsies.

20 nalyzed circulating cytokine levels in ALK(+)ALCL patients and detected elevated levels of IL-22, IL-

21 es the involvement of IL-22R1/IL-22 in ALK(+)ALCL.

22 e relationship between the ALK(+) and ALK(-) ALCL subtypes, we performed a genome-wide DNA profiling

23 Cases of ALK(+) ALCL and ALK(-) ALCL were interspersed in unsupervised analysis, suggest

24 ns involving the ALK gene (ALK(+) and ALK(-) ALCL).

25 notypic or genetic features to define ALK(-) ALCL are missing, and their distinction from other T-cel

26 miR-143, miR-494) that differentiates ALK(-) ALCL from other PTCLs.

27 samples of primary NPM-ALK(+) and NPM-ALK(-) ALCL to investigate the role of miR-150 downstream of NP

28 m set of genes capable of recognizing ALK(-) ALCL.

29 TMOD1) able to successfully separate ALK(-) ALCL from peripheral T-cell lymphoma not otherwise speci

30 were also discovered in WT JAK1/STAT3 ALK(-) ALCL.

31 re frequently, but not exclusively, in ALK(-)ALCL.

32 53 and/or PRDM1 were present in 52% of ALK(-)ALCL, and in 29% of all ALCL cases with a clinical impli

33 ALK+ ALCL typically occurs in younger patients and has a more

34 y) had no effect on cell viability of 2 ALK+ ALCL cell lines, Karpas 299 and SU-DHL1, each expressing

35 In 26 ALK+ ALCL tumors, assessed for expression of DISC-associated

36 expression of IL-9Ralpha and IL-9 in 3 ALK+ ALCL-cell lines and 75% and 83% of primary tumors, respe

37 indistinguishable from patient-derived ALK+ ALCL.

38 rs may have therapeutic application for ALK+ ALCL and possibly other solid and hematologic tumors in

39 erum-free culture medium harvested from ALK+ ALCL-cell lines, supporting autocrine release of IL-9.

40 rotein S6, are highly phosphorylated in ALK+ ALCL cell lines and tumors.

41 uced cell cycle arrest and apoptosis in ALK+ ALCL cells.

42 iptional effector GLI1, is amplified in ALK+ ALCL tumors and cell lines, and that SHH and GLI1 protei

43 d GLI1 proteins are highly expressed in ALK+ ALCL tumors and cell lines.

44 ed that IL-9 plays an important role in ALK+ ALCL via Jak3 activation.

45 /GLI1 signaling pathway is activated in ALK+ ALCL.

46 ogenic effects of activated PI3K/AKT in ALK+ ALCL.

47 nts a potential therapeutic strategy in ALK+ ALCL.

48 eve a more potent therapeutic effect in ALK+ ALCL.

49 large cell lymphoma (ALCL) morphology (ALK+ ALCL), the vast majority of which harbor the well-charac

50 rmed CD4+ T lymphocytes and primary NPM-ALK+ ALCL biopsies share similarities with early T cell precu

51 significant role in the pathogenesis of ALK+ ALCL and that it represents a potential therapeutic targ

52 l for the proliferation and survival of ALK+ ALCL cells in culture.

53 sed cell viability and clonogenicity of ALK+ ALCL cells.

54 arget for the therapeutic modulation of ALK+ ALCL has not been validated thus far.

55 component of the favorable prognosis of ALK+ ALCL.

56 that overexpression of c-FLIP protects ALK+ ALCL cells from death-receptor-induced apoptosis and may

57 st majority of children with high-stage ALK+ ALCL.

58 ition of NPM-ALK phosphorylation in the ALK+ ALCL-derived cell lines resulted in significant inhibiti

59 location and a survival rate similar to ALK+ ALCL or a less common P63 translocation, the latter asso

60 eutic target for treating patients with ALK+ ALCL.

61 ctively expressed in neoplastic cells of ALK+ALCL tissue biopsies, and showed a significant correlati

62 Anaplastic lymphoma kinase-positive (ALK+) ALCL is associated with the NPM-ALK t(2;5) translocation

63 n anaplastic lymphoma kinase-positive (ALK+) ALCL, WASP and WIP expression is regulated by ALK oncoge

64 taneous ALCL and systemic type ALK+ and ALK- ALCL.

65 inical application of targeting JAK for ALK- ALCL, we treated ALK- cell lines of various histological

66 rrent translocations were identified in ALK- ALCL.

67 tumor cell survival in diverse forms of ALK- ALCL, even in the presence of JAK1/STAT3 mutations.

68 ted in cell lines as well as in primary ALK- ALCL tumors.

69 wever, emerging data now highlight that ALK- ALCL is genetically and clinically heterogeneous with a

70 tor therapy might benefit patients with ALK- ALCL who are phosphorylated STAT3<sup/>.

71 ystemic ALCL, but in many patients with ALK- ALCL, it is ineffective, and thus it is often followed b

72 r, was effective in vivo in a xenograft ALK- ALCL model.

73 Conversely, ALK-ALCL tissue biopsies did not show significant correlatio

74 ison with 40% to 60% for ALK-negative (ALK-) ALCL.

75 sent in 52% of ALK(-)ALCL, and in 29% of all ALCL cases with a clinical implication.

76 nical trials conducted with SGN-30 in HD and ALCL.

77 o clinical responses in patients with HL and ALCL, indicating that further assessment of this therapy

78 patients with relapsed Hodgkin lymphoma and ALCL.

79 Most patients with breast implant-associated ALCL who had disease confined within the fibrous capsule

80 ging studies in immunodeficient mice bearing ALCL xenotransplants were carried out with the cell line

81 nd 19 in situ subtypes) collected from 54 BI-ALCL patients diagnosed through the French Lymphopath ne

82 ssociated anaplastic large cell lymphoma (BI-ALCL) remain elusive.

83 One case of BI-ALCL is reported.

84 Our results show that the BI-ALCL genomic landscape is characterized by not only JAK/

85 BIA-ALCL incidence and incidence rates may be higher than pr

86 Time-to-event analysis demonstrated a BIA-ALCL cumulative incidence of 0 at up to 6 years, increas

87 patients and healthcare providers about BIA-ALCL, we convened to review diagnostic procedures used i

88 ndance of Gram-negative bacteria between BIA-ALCL and control specimens.

89 ota did not differ significantly between BIA-ALCL and controls for any material analyzed.

90 implants to distinguish seroma caused by BIA-ALCL from other causes of seroma accumulation, such as i

91 clonal T-cell proliferation and clinical BIA-ALCL.

92 ients with no clear trend to distinguish BIA-ALCL from controls.

93 Almost all documented BIA-ALCL cases have been associated with a textured device.

94 To assess how BIA-ALCL develops, its risk factors, diagnosis, and subseque

95 of breast, skin, implant and capsule in BIA-ALCL patients (n = 7), and controls via culturing method

96 characteristic loss of chromosome 20 in BIA-ALCL provides further justification to recognize BIA-ALC

97 deregulation is significantly higher in BIA-ALCL, as indicated by phosphorylated STAT3 immunohistoch

98 ng JAK proteins warrant investigation in BIA-ALCL.

99 sociated anaplastic large cell lymphoma (BIA-ALCL) at a high-volume single institution, which enables

100 sociated anaplastic large-cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-neg

101 sociated anaplastic large cell lymphoma (BIA-ALCL) is a very rare type of T-cell lymphoma that is uni

102 sociated anaplastic large cell lymphoma (BIA-ALCL), a CD30+ T-cell lymphoma associated with textured

103 sociated anaplastic large cell lymphoma (BIA-ALCL), a rare peripheral T-cell lymphoma, is increasing

104 analysis of a relatively large series of BIA-ALCL (n = 29), for which genome-wide chromosomal copy nu

105 Cytokine expression profiling of BIA-ALCL cell lines and clinical specimens reveals a predomi

106 Loss of 20q13.13 is characteristic of BIA-ALCL compared with other classes of ALCL, such as primar

107 The reported incidence of BIA-ALCL is highly variable, ranging from 1 in 355 to 1 in 3

108 Early diagnosis of BIA-ALCL is important as the disease can progress and deaths

109 Because the most common presentation of BIA-ALCL is swelling of the breast with fluid collection, an

110 The overall incidence of BIA-ALCL was 1.79 per 1000 patients (1 in 559) with textured

111 The incidence and incidence rate of BIA-ALCL were estimated per patient and per implant.

112 ated mast cells in clinical specimens of BIA-ALCL.

113 view summarizes the current knowledge on BIA-ALCL cell of origin and immunologic factors underlying i

114 Data on BIA-ALCL, such as pathophysiology, patient demographics, pre

115 vides further justification to recognize BIA-ALCL as a separate disease entity.

116 he evaluation of patients with suspected BIA-ALCL.

117 evaluation of the patient with suspected BIA-ALCL.

118 ed microbes, were identified in both the BIA-ALCL and contralateral control breast.

119 cles, and any other articles relevant to BIA-ALCL were included.

120 stimulus, possibly infectious, triggers BIA-ALCL.

121 n have been detected and associated with BIA-ALCL pathogenesis in a small number of cases.

122 Eleven patients were diagnosed with BIA-ALCL, all of whom had a history of textured implants.

123 istent differences between patients with BIA-ALCL-affected and contralateral control breasts, this st

124 Consistently, in both ALCL and NSCLC, we found that under hypoxic conditions,

125 main open regarding the pathogenesis of both ALCL subtypes.

126 Children affected by ALCL may thus harbour thymic lymphoma-initiating cells c

127 cases, and raised RB1 expression in 7 of 8 C-ALCL.

128 eous CD30+ anaplastic large-cell lymphoma (C-ALCL).

129 BCL1 expression was seen in nine MF, seven C-ALCL, and six SS cases.

130 pharmacologic inhibition partially controls ALCL cell growth and disease progression in an ERBB4-pos

131 r classes of ALCL, such as primary cutaneous ALCL and systemic type ALK+ and ALK- ALCL.

132 Herein we describe ALCL cells expressing truncated forms of the CD30 intrac

133 In this review, we briefly discuss ALCL and focus on NPM-ALK.

134 ne, suggesting its potential application for ALCL-specific cancer treatment.

135 MYC, itself, is essential for ALCL survival, as both knockdown of MYC and pharmacologi

136 epresent a preferable therapeutic option for ALCL treatment.

137 F2alpha, but not HIF1alpha, was required for ALCL growth in vivo whereas the growth and metastasis po

138 apoptotic cell death in vitro, and hindered ALCL tumorigenic potential in vivo.

139 timating expression levels in cultured human ALCL cells, a key tool in ALCL pathobiology research.

140 confirmed these findings derived from human ALCL cells in murine pro-B cells that were transformed t

141 ith this, clonal TCR rearrangements in human ALCL are predominantly in-frame, but often aberrant, wit

142 recognizes CD25, in a murine model of human ALCL.

143 VEGFA antibody bevacizumab strongly impaired ALCL growth in mouse xenografts.

144 men with cytologically proven breast implant ALCL from 2014 to 2019.

145 e, treatment, and outcomes in breast implant ALCL patients.

146 Robust participation in the breast implant ALCL PROFILE registry will improve our knowledge of long

147 ing database of patients with breast implant ALCL will further improve our understanding of the disea

148 aplastic large cell lymphoma (breast implant ALCL) is an uncommon T cell lymphoma, which is associate

149 utline the clinical course of breast implant ALCL.

150 with pathologically confirmed breast implant ALCL.

151 In ALCL, the upregulation of HIF1alpha and HIF2alpha in hyp

152 signaling pathway and STAT3 is activated in ALCL, survivin expression was also correlated with STAT3

153 onstrate that inhibition of pAkt activity in ALCL decreases p27 phosphorylation and degradation, resu

154 is the key mechanism of ALK-TKI addiction in ALCL.

155 reveal the mechanism of ALK-TKI addiction in ALCL.

156 was toxic to ALCL cell lines in vitro and in ALCL xenograft mouse models in vivo.

157 d VEGFA production and tumor angiogenesis in ALCL and NSCLC, and the treatment with the anti-VEGFA an

158 s last activity is much less well defined in ALCL cells.

159 od to modulate NPM-ALK protein expression in ALCL-derived, t(2;5)-positive Karpas 299 cells.

160 hat that PRDM1 is a tumor suppressor gene in ALCL models, likely acting as an antiapoptotic agent.

161 YC expression and its target gene network in ALCL.

162 ary for CD30-driven growth arrest signals in ALCL cells.

163 These data reveal that in ALCL cells, in contrast to other cell types, CD30 stimul

164 in cultured human ALCL cells, a key tool in ALCL pathobiology research.

165 filing meta-analysis of 309 cases, including ALCL and other primary T-NHL samples.

166 ylation, rescued TSG expression, and induced ALCL apoptotic cell death.

167 ng SIN3A caused reexpression of TSG, induced ALCL apoptotic cell death in vitro, and hindered ALCL tu

168 regulated on anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) cells.

169 most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymphoma.

170 cers such as anaplastic large-cell lymphoma (ALCL) and inflammatory myofibroblastic tumor (IMT).

171 s, including anaplastic large-cell lymphoma (ALCL) and non-small cell lung carcinoma (NSCLC).

172 cogenesis of anaplastic large cell lymphoma (ALCL) are not completely understood.

173 (NPM-ALK(+)) anaplastic large-cell lymphoma (ALCL) as model system, we found in cells and patient-der

174 Most of the anaplastic large-cell lymphoma (ALCL) cases carry the t(2;5; p23;q35) that produces the

175 ly in ALK(+) anaplastic large cell lymphoma (ALCL) cell lines and primary tumours.

176 ALK-positive anaplastic large cell lymphoma (ALCL) cell lines to evaluate two inhibitors, the HSP90 i

177 s, including anaplastic large cell lymphoma (ALCL) cells.

178 or absent in anaplastic large cell lymphoma (ALCL) compared to other T cell lymphomas.

179 LK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ideal model disease to study tumor-

180 LK)-positive anaplastic large cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35) resulting i

181 Anaplastic large-cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35), resulting

182 oma (HL) and anaplastic large cell lymphoma (ALCL) has had profound clinical success.

183 hogenesis of anaplastic large-cell lymphoma (ALCL) have been well defined; nevertheless, the notion t

184 LK)-negative anaplastic large cell lymphoma (ALCL) is a CD30-positive T-cell non-Hodgkin lymphoma tha

185 Anaplastic large-cell lymphoma (ALCL) is a clinical and biological heterogeneous disease

186 Anaplastic large cell lymphoma (ALCL) is a distinct entity of T-cell lymphoma that can b

187 Anaplastic large cell lymphoma (ALCL) is a mature T cell neoplasm that often expresses t

188 Anaplastic large cell lymphoma (ALCL) is a mature T-cell lymphoma that can present as a

189 Anaplastic large cell lymphoma (ALCL) is a peripheral T-cell lymphoma presenting mostly

190 t-associated anaplastic large-cell lymphoma (ALCL) is a recently described clinicopathologic entity t

191 Systemic anaplastic large-cell lymphoma (ALCL) is a T-cell lymphoma, whose anaplastic lymphoma ki

192 Systemic anaplastic large cell lymphoma (ALCL) is an aggressive CD30(+) non-Hodgkin lymphoma.

193 Systemic anaplastic large-cell lymphoma (ALCL) is an aggressive subtype of T-cell lymphoma charac

194 Systemic anaplastic large cell lymphoma (ALCL) is an aggressive T-cell lymphoma most commonly see

195 Anaplastic large cell lymphoma (ALCL) is the most common type of pediatric peripheral T-

196 hogenesis of anaplastic large-cell lymphoma (ALCL) is unknown.

197 hogenesis of anaplastic large-cell lymphoma (ALCL) is well established.

198 mphomas with anaplastic large cell lymphoma (ALCL) morphology (ALK+ ALCL), the vast majority of which

199 ive (ALK(+)) anaplastic large cell lymphoma (ALCL) patients.

200 Anaplastic large-cell lymphoma (ALCL) represents a heterogeneous group of aggressive non

201 ALK-positive anaplastic large-cell lymphoma (ALCL) resistant to ALK-specific tyrosine kinase inhibito

202 mas, such as anaplastic large-cell lymphoma (ALCL) tumors.

203 K) -positive anaplastic large-cell lymphoma (ALCL) was excluded.

204 Anaplastic large-cell lymphoma (ALCL) was initially recognized on the basis of morpholog

205 K-rearranged anaplastic large cell lymphoma (ALCL), a specific subtype of T-cell lymphoma, the Rho fa

206 ive (ALK(+)) anaplastic large-cell lymphoma (ALCL), and adult T-cell leukemia/lymphoma.

207 , three with anaplastic large-cell lymphoma (ALCL), and two with CD30+ T-cell lymphoma--were enrolled

208 and systemic anaplastic large cell lymphoma (ALCL), the single agent response rates were 75 and 86%,

209 oma (HL) and anaplastic large-cell lymphoma (ALCL), the study by Jacobsen and colleagues in this issu

210 0% to 70% of anaplastic large cell lymphoma (ALCL), which is a T/null cell non-Hodgkin's lymphoma sho

211 rotein in an anaplastic large cell lymphoma (ALCL)-derived cell line carrying the t(2;5)(p23;q35), an

212 LK)-positive anaplastic large-cell lymphoma (ALCL).

213 and systemic anaplastic large cell lymphoma (ALCL).

214 al models of anaplastic large cell lymphoma (ALCL).

215 LK)-positive anaplastic large cell lymphoma (ALCL).

216 ase (HD) and anaplastic large cell lymphoma (ALCL).

217 ALK-positive anaplastic large-cell lymphoma (ALCL).

218 role in ALK+ anaplastic large-cell lymphoma (ALCL).

219 esis in ALK+ anaplastic large-cell lymphoma (ALCL).

220 /R) systemic anaplastic large cell lymphoma (ALCL).

221 [AITL], and anaplastic large-cell lymphoma [ALCL]) is difficult, with the morphologic and phenotypic

222 g pediatric anaplastic large cell lymphomas (ALCL) and inflammatory myofibroblastic tumors (IMTs).

223 tely 70% of anaplastic large cell lymphomas (ALCL).

224 oprotein in anaplastic large cell lymphomas (ALCL).

225 Karpas-299 (anaplastic large-cell lymphomas [ALCL]) and H3122 (NSCLC).

226 rrent translocation reported in ALK-negative ALCL and highlight the utility of massively parallel gen

227 we identified a new subclass of ALK-negative ALCL characterized by aberrant expression of ERBB4-trunc

228 discriminating either AITL and ALK-negative ALCL from PTCL NOS in a training set.

229 it enhanced the distinction of ALK-negative ALCL from PTCL NOS, especially from some CD30+ PTCL NOS

230 c and clinical heterogeneity of ALK-negative ALCL has not been delineated.

231 77% for AITL and 98% to 93% for ALK-negative ALCL in test and validation sets of patient cases, respe

232 Thus, ALK-negative ALCL is a genetically heterogeneous disease with widely

233 arkers and/or genes involved in ALK-negative ALCL pathogenesis, we applied the cancer outlier profile

234 ve ALCL patients but not in two ALK-negative ALCL patients or five normal subjects.

235 A1 genes was detected in 24% of ALK-negative ALCL patients.

236 patients with ALK-positive and ALK-negative ALCL, beta(2)-microglobulin was >/= 3 mg/L in 12% and 33

237 Best results were obtained in ALK-negative ALCL.

238 le site on 7q32.3 in a systemic ALK-negative ALCL.

239 that t(2;5)(p23;q35) occurs in 40% to 60% of ALCL patients established a distinct clinicopathologic e

240 a comprehensive phosphoproteome analysis of ALCL cell lines was performed in the presence or absence

241 c of BIA-ALCL compared with other classes of ALCL, such as primary cutaneous ALCL and systemic type A

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

243 We show that a fraction of ALCL cells rapidly underwent apoptosis following CD30 st

244 tein receptor as essential for the growth of ALCL cells in culture and as patient-derived xenografts.

245 tor, NVP-TAE684, which blocked the growth of ALCL-derived and ALK-dependent cell lines with IC(50) va

246 n regulating invasiveness and oncogenesis of ALCL.

247 nd Rac1 control rather similar phenotypes of ALCL biology such as the proliferation, survival, and mi

248 ft model and enhances invasive properties of ALCL.

249 Using this system, CD30 was stimulated on ALCL and HL cells, and the subsequent CD30 signaling pro

250 ch 9 patients with relapsed/refractory HL or ALCL were infused with autologous T cells that were gene

251 of uniformly treated ALK-positive pediatric ALCL patients to ascertain whether the titers of preexis

252 Here we present a model of peripheral ALCL pathogenesis where the malignancy is initiated in e

253 tients with relapsed/refractory ALK-positive ALCL and 14 patients with metastatic or inoperable ALK-p

254 is in two independent models of ALK-positive ALCL and induced regression of established Karpas-299 ly

255 ism of cancer drug addiction in ALK-positive ALCL and the benefit of scheduled intermittent dosing in

256 that morphologically resembles ALK-positive ALCL but lacks chromosomal rearrangements of the ALK gen

257 CD4(+) Th cell lines lysed ALK-positive ALCL cell lines in a MHC class II-restricted manner.

258 Early evaluation of MRD in NPM-ALK-positive ALCL identifies patients with a very high relapse risk a

259 provide novel insights into NPM/ALK-positive ALCL pathobiology.

260 6), as being immunogenic in six ALK-positive ALCL patients but not in two ALK-negative ALCL patients

261 e immunotherapeutic options for ALK-positive ALCL patients who fail to respond well to conventional t

262 ave previously been detected in ALK-positive ALCL patients, their prognostic significance is unknown.

263 Moreover, a novel NPM1-ALK-positive ALCL PDX model showed a significant survival benefit fro

264 marrow of 180 patients with NPM-ALK-positive ALCL treated with Berlin-Frankfurt-Munster-type protocol

265 fficacy when dosed orally in an ALK-positive ALCL tumor xenograft model in SCID mice, warranting furt

266 ence of a CD4(+) Th response in ALK-positive ALCL.

267 ically active in both cell lines and primary ALCL, whereas the nuclear portion was inactive because o

268 ere significantly enriched in ALK-rearranged ALCL and NSCLC, as compared with other types of T-cell l

269 pecific therapeutic target in ALK-rearranged ALCL and NSCLC.

270 We found that in ALK-rearranged ALCL cell lines, NPM-ALK was distributed in equal amount

271 2 or Rac1 in a mouse model of ALK-rearranged ALCL to show that either Cdc42 or Rac1 deletion impaired

272 nd durable remissions in relapsed/refractory ALCL and is under investigation in the first-line settin

273 For early relapsed ALCL autologous SCT was not effective.

274 crizotinib therapy in patients with relapsed ALCL and metastatic or unresectable IMT highlight the im

275 , in contrast to NSCLC cells, drug-resistant ALCL cells show no evidence of bypassing ALK by activati

276 a chance for cure in patients with high-risk ALCL relapse.

277 With prolonged CD30 stimulation, ALCL cells underwent cell cycle arrest that correlated w

278 The surviving ALCL cells exhibited robust activation of both the canon

279 Systemic ALCL represents 2% to 5% of adult lymphoma but up to 30%

280 efinement of the prognosis of adult systemic ALCL, with ALK prognostic value dependent on age, and co

281 tive clinical trials with confirmed systemic ALCL after immunohistopathologic review and defined ALK

282 ard first-line treatment choice for systemic ALCL, but in many patients with ALK- ALCL, it is ineffec

283 Two subtypes of systemic ALCL are currently recognized on the basis of the presen

284 han half of patients with recurrent systemic ALCL.

285 reatment for relapsed or refractory systemic ALCL and warrants further studies in front-line therapy.

286 atients with relapsed or refractory systemic ALCL, provide evidence that single-agent brentuximab ved

287 atients with relapsed or refractory systemic ALCL.

288 The ALCL model was established by intravenous injection of k

289 The ALCL-Relapse trial (ClinicalTrials.gov identifier: NCT00

290 eks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRgamma(-/

291 solid tumors and found it does not apply to ALCL.

292 ptor-induced apoptosis and may contribute to ALCL pathogenesis.

293 own of IRF4 by RNA interference was toxic to ALCL cell lines in vitro and in ALCL xenograft mouse mod

294 ic inhibition of MYC signaling were toxic to ALCL cell lines.

295 tional 51 patients, 47 with HL and four with ALCL, were treated at doses of 1, 5, 10, and 15 mg/kg.

296 The overall response rates for patients with ALCL treated at doses of 165 (ALCL165) and 280 (ALCL280)

297 Of 2 patients with ALCL, 1 had a CR that persisted 9 months after the fourt

298 Among the 138 adult patients with ALCL, 64 (46%) were ALK positive, and 74 (54%) were ALK

299 NPM-ALK fusion transcripts in patients with ALCL.

300 creased during therapy in most patients with ALCL.