ライフサイエンスコーパス: anaplastic

1 ht desmoplastic-nodular, two large cell, one anaplastic), 17 ependymomas (13 World Health Organizatio

2 s 4.5% (42% papillary, 42% follicular and 8% anaplastic), and the yield of malignancy decreased consi

3 Nine atypical, three anaplastic, and 39 typical meningiomas were retrospectiv

4 are subtypes of thyroid cancer-medullary and anaplastic-are ideally treated by physicians with experi

5 both IDH-mt and 1p/19q co-deletion, whereas anaplastic astrocytoma is divided into IDH wild-type ( I

6 Anaplastic astrocytoma samples with mutated IDH1 display

7 n levels were significantly higher in GB and anaplastic astrocytoma tissues than in grade II glioma a

8 erms glioblastoma, glioma, malignant glioma, anaplastic astrocytoma, anaplastic oligodendroglioma, an

9 tomas, 1 anaplastic oligodendroglioma, and 1 anaplastic astrocytoma.

10 ocytoma (IMA) cell line from a WHO grade III anaplastic astrocytoma.

11 ioma, 1 had anaplastic ependymoma, and 1 had anaplastic astrocytoma.

12 rbations that yield high-grade astrocytomas (anaplastic astrocytomas and GBMs).

13 om World Health Organization (WHO) grade III anaplastic astrocytomas to WHO grade IV glioblastomas.

14 ls) were included (5 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 gliomatosis cerebri, and 1 gl

15 cell cancer of the right lung (microcellular anaplastic carcinoma), was admitted with focal neurologi

16 was associated with aggressive medullary and anaplastic carcinomas, and its expression pattern in med

17 -expression profile is enriched in advanced, anaplastic, castration-resistant and metastatic prostate

18 27 trimethylation, is overexpressed in CD30+ anaplastic cells in primary cutaneous anaplastic T-cell

19 roliferation, and led to retinoblastoma with anaplastic changes.

20 en deletion show increased proliferation and anaplastic dedifferentiation, as well as mTORC1 hyperact

21 died from a secondary tumour (head and neck anaplastic embryonal rhabdomyosarcoma), all patients wer

22 e, 2 had anaplastic oligodendroglioma, 1 had anaplastic ependymoma, and 1 had anaplastic astrocytoma.

23 % at all times for ependymomas WHO I/II, for anaplastic ependymomas WHO III 100%, 100%, 70% and 100%,

24 free survival was 24 weeks for patients with anaplastic glioma (95% CI, 5 to 31 weeks) and 12 weeks f

25 reased OEF (+18%, P < .001, n = 20), whereas anaplastic glioma (WHO grade III) and glioblastoma (WHO

26 reation of a timely diagnostic algorithm for anaplastic glioma based on multivariable analysis of con

27 e undergone malignant progression (MP) to an anaplastic glioma or secondary glioblastoma (GBM).

28 older and had newly diagnosed non-co-deleted anaplastic glioma with WHO performance status scores of

29 te was 24% (18% for glioblastoma and 44% for anaplastic glioma).

30 vity in patients with temozolomide-resistant anaplastic glioma, but there seemed to be no significant

31 patients with newly diagnosed non-co-deleted anaplastic glioma.

32 lioblastoma cohort and 25% for patients with anaplastic glioma.

33 Anaplastic gliomas, the most common and malignant of pri

34 apy in newly diagnosed 1p/19q non-co-deleted anaplastic gliomas, which are associated with lower sens

35 w-grade fibrillary astrocytoma to high-grade anaplastic gliomas.

36 t temozolomide in adults with non-co-deleted anaplastic gliomas.

37 t side of her vision, due to a WHO grade III anaplastic haemangiopericytoma compressing the optic chi

38 y number was associated with the presence of anaplastic histologic features and shorter survival in m

39 Of the 6 patients who died, 5 had diffuse anaplastic histology.

40 itors induced tumors exhibiting a large-cell/anaplastic histopathology adjacent to the fourth ventric

41 vasion and contributes to the oncogenesis of anaplastic large cell lymphoma (ALCL) are not completely

42 We used various ALK-positive anaplastic large cell lymphoma (ALCL) cell lines to eval

43 normal and malignant lymphocytes, including anaplastic large cell lymphoma (ALCL) cells.

44 Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ide

45 onal antibodies in Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL) has had profound c

46 Anaplastic lymphoma kinase (ALK)-negative anaplastic large cell lymphoma (ALCL) is a CD30-positive

47 Anaplastic large cell lymphoma (ALCL) is a distinct enti

48 Anaplastic large cell lymphoma (ALCL) is a mature T-cell

49 Anaplastic large cell lymphoma (ALCL) is a peripheral T-

50 Systemic anaplastic large cell lymphoma (ALCL) is an aggressive C

51 Anaplastic large cell lymphoma (ALCL) is the most common

52 ntified in a subset of T-cell lymphomas with anaplastic large cell lymphoma (ALCL) morphology (ALK+ A

53 anaplastic lymphoma kinase-positive (ALK(+)) anaplastic large cell lymphoma (ALCL) patients.

54 In ALK-rearranged anaplastic large cell lymphoma (ALCL), a specific subtyp

55 with relapsed Hodgkin lymphoma and systemic anaplastic large cell lymphoma (ALCL), the single agent

56 s with relapsed or refractory (R/R) systemic anaplastic large cell lymphoma (ALCL).

57 nt of relapsed Hodgkin lymphoma and systemic anaplastic large cell lymphoma (ALCL).

58 were orally efficacious in animal models of anaplastic large cell lymphoma (ALCL).

59 nd anaplastic lymphoma kinase (ALK)-negative anaplastic large cell lymphoma (ALK-negative), despite t

60 Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL), a rare periph

61 signature was robust enough to differentiate anaplastic large cell lymphoma (n = 32) from other PTCLs

62 plastic lymphoma kinase (NPM-ALK) expressing anaplastic large cell lymphoma are not completely unders

63 chromosome breaks and translocations in the anaplastic large cell lymphoma breakpoint regions of NPM

64 ymphoma kinase (ALK)-positive and -negative, anaplastic large cell lymphoma cell lines and primary pa

65 optotic anaplastic lymphoma kinase-positive, anaplastic large cell lymphoma cell lines and that ectop

66 Breast implant-associated anaplastic large cell lymphoma is a rare cancer in patie

67 nerated to target different receptors on the anaplastic large cell lymphoma line L-82, but delivered

68 rmed mycosis fungoides (T-MF), and cutaneous anaplastic large cell lymphoma were studied in parallel

69 xcluding anaplastic lymphoma kinase-positive anaplastic large cell lymphoma), upfront auto-SCT was as

70 ma kinase (ALK)-positive and 48 ALK-negative anaplastic large cell lymphoma, 14 adult T-cell leukemia

71 g PTCL NOS, angioimmunoblastic, ALK-negative anaplastic large cell lymphoma, and enteropathy-associat

72 diffuse large B-cell lymphoma, ALK-positive anaplastic large cell lymphoma, chronic myelogenous leuk

73 sed or refractory Hodgkin lymphoma, systemic anaplastic large cell lymphoma, relapsed or refractory B

74 , including rhabdomyosarcoma, neuroblastoma, anaplastic large cell lymphoma, renal cell carcinoma, an

75 oides, Sezary syndrome, or primary cutaneous anaplastic large cell lymphoma, with disease progression

76 phase 2 trials in CD30+ Hodgkin lymphoma and anaplastic large cell lymphoma.

77 es, including classical Hodgkin lymphoma and anaplastic large cell lymphoma.

78 dominant genetic lesion underlying pediatric anaplastic large cell lymphomas (ALCL) and inflammatory

79 ung cancers (NSCLC) and approximately 70% of anaplastic large cell lymphomas (ALCL).

80 ncluding anaplastic lymphoma kinase (ALK)(-) anaplastic large cell lymphomas (ALCLs).

81 ving ALK, occurring in approximately half of anaplastic large cell lymphomas (ALCLs).

82 e treatment of relapsed Hodgkin and systemic anaplastic large cell lymphomas--both characterized by h

83 30-expressing Classical Hodgkin and systemic anaplastic large cell lymphomas.

84 lymphoma cell lines, including mantle cell, anaplastic large cell, and Hodgkin lymphoma cell lines.

85 T cell not otherwise specified; 2 (13%) had anaplastic large cell; and 1 each had extranodal natural

86 T-cell lymphoma, characterized by the CD30+ anaplastic large T cells, comprises the second most comm

87 d, refractory Hodgkin lymphomas and systemic anaplastic large T-cell lymphomas.

88 apy-sensitive disease (86% v 60%; P < .001), anaplastic large-cell histology (53% v 40%; P = .04), an

89 us lymphoid-derived neoplasias, most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymp

90 defining events in several tumors, including anaplastic large-cell lymphoma (ALCL) and non-small cell

91 Most of the anaplastic large-cell lymphoma (ALCL) cases carry the t(

92 Anaplastic large-cell lymphoma (ALCL) is a clinical and

93 Breast implant-associated anaplastic large-cell lymphoma (ALCL) is a recently desc

94 Systemic anaplastic large-cell lymphoma (ALCL) is a T-cell lympho

95 Systemic anaplastic large-cell lymphoma (ALCL) is an aggressive s

96 and is downregulated in T-lymphomas, such as anaplastic large-cell lymphoma (ALCL) tumors.

97 Anaplastic lymphoma kinase (ALK) -positive anaplastic large-cell lymphoma (ALCL) was excluded.

98 t of patients with Hodgkin lymphoma (HL) and anaplastic large-cell lymphoma (ALCL), the study by Jaco

99 th anaplastic lymphoma kinase (ALK)-positive anaplastic large-cell lymphoma (ALCL).

100 Anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma (ALK(+) ALCL) is a unique

101 7), adult T-cell lymphoma/leukemia (n = 4), anaplastic large-cell lymphoma (n = 2), and extranodal n

102 gioimmunoblastic T-cell lymphoma [AITL], and anaplastic large-cell lymphoma [ALCL]) is difficult, wit

103 All seven patients without anaplastic large-cell lymphoma achieved CR.

104 harbouring ALK translocations, particularly anaplastic large-cell lymphoma and inflammatory myofibro

105 e aberrantly expressed in a subset of T-cell anaplastic large-cell lymphoma and non-small-cell lung c

106 Hodgkin's lymphoma and anaplastic large-cell lymphoma are the two most common t

107 e treatment of relapsed Hodgkin lymphoma and anaplastic large-cell lymphoma by the Food and Drug Admi

108 for select patients, particularly those with anaplastic large-cell lymphoma histology.

109 In T-cell lymphomas, anaplastic large-cell lymphoma is defined by mutually ex

110 itive mycosis fungoides or primary cutaneous anaplastic large-cell lymphoma who had been previously t

111 RC1; and expression of CD30 (the hallmark of anaplastic large-cell lymphoma) and of immunosuppressive

112 Outcomes of 241 patients (112 anaplastic large-cell lymphoma, 102 peripheral T-cell ly

113 of PTCL not otherwise specified (PTCL-NOS), anaplastic large-cell lymphoma, and adult T-cell leukemi

114 We also examine T-cell lymphomas, including anaplastic large-cell lymphoma, angioimmunoblastic T-cel

115 In contrast to Hodgkin lymphoma and systemic anaplastic large-cell lymphoma, CD30 expression of malig

116 lifications, or oncogenic mutations, such as anaplastic large-cell lymphoma, inflammatory myofibrobla

117 tivating ALK aberrations (eight of nine with anaplastic large-cell lymphoma, one of 11 with neuroblas

118 urable or evaluable solid or CNS tumours, or anaplastic large-cell lymphoma, refractory to therapy an

119 target in patients with Hodgkin lymphoma and anaplastic large-cell lymphoma.

120 n children with refractory solid tumours and anaplastic large-cell lymphoma.

121 ne marrow and blood samples of patients with anaplastic large-cell lymphoma.

122 ic cancers, primarily Hodgkin's lymphoma and anaplastic large-cell lymphoma.

123 a (ENKCL), and ATLL and a lower incidence of anaplastic large-cell lymphoma; Hispanics had a higher i

124 Anaplastic large-cell lymphomas (ALCLs) are a group of c

125 Anaplastic large-cell lymphomas (ALCLs) bearing the t(2;

126 Anaplastic large-cell lymphomas (ALCLs) encompass at lea

127 K+ xenografts in mice, including Karpas-299 (anaplastic large-cell lymphomas [ALCL]) and H3122 (NSCLC

128 In addition to 100% anaplastic large-cell lymphomas, 57% of other PTCL entit

129 n of tumors indistinguishable from patients' anaplastic large-cell lymphomas.

130 ophenotype characteristic of patient-derived anaplastic large-cell lymphomas.

131 atients with relapsed or refractory systemic anaplastic large-T-cell lymphoma who previously received

132 relapsed or refractory Hodgkin's lymphoma or anaplastic large-T-cell lymphoma, had biopsy-proven CD30

133 elapsed or refractory Hodgkin's lymphoma and anaplastic large-T-cell lymphoma.

134 %] with Hodgkin's lymphoma and one [2%] with anaplastic large-T-cell lymphoma; 28 [43%] during phase

135 Metastatic disease and large-cell/anaplastic (LC/A) phenotype were the clinicopathologic v

136 ly of SHH and displays classic or large cell anaplastic (LCA) pathology and poor prognosis.

137 ide 1 was identified as a novel inhibitor of anaplastic lymphoma kinase (ALK enzyme assay IC(50) = 0.

138 Anaplastic lymphoma kinase (ALK) -positive anaplastic la

139 Anaplastic lymphoma kinase (Alk) and leucocyte tyrosine

140 belly (Jeb) and its receptor tyrosine kinase Anaplastic lymphoma kinase (Alk) are localized to develo

141 ncogenic fusion genes consisting of EML4 and anaplastic lymphoma kinase (ALK) are present in a subgro

142 The phylogenetic proximity of the ROS1 and anaplastic lymphoma kinase (ALK) catalytic domains led t

143 Anaplastic lymphoma kinase (ALK) constitutes a part of t

144 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) define two unique subty

145 We demonstrate that anaplastic lymphoma kinase (Alk) efficiently protects ne

146 lymphoma (ALCL) is a T-cell lymphoma, whose anaplastic lymphoma kinase (ALK) expression varies accor

147 distinguished by the presence or absence of anaplastic lymphoma kinase (ALK) expression.

148 This review describes the identification of anaplastic lymphoma kinase (ALK) fusion genes in approxi

149 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion oncogene represe

150 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion protein, presume

151 Rearrangements involving the anaplastic lymphoma kinase (ALK) gene are defining event

152 d here to detection of rearrangements in the anaplastic lymphoma kinase (ALK) gene associated with AL

153 he discovery of rearrangements involving the anaplastic lymphoma kinase (ALK) gene in thyroid cancer.

154 Molecular testing is positive for an anaplastic lymphoma kinase (ALK) gene rearrangement usin

155 In 2007, scientists discovered that anaplastic lymphoma kinase (ALK) gene rearrangements are

156 Anaplastic lymphoma kinase (ALK) gene rearrangements are

157 dermal growth factor receptor (EGFR) gene or anaplastic lymphoma kinase (ALK) gene rearrangements.

158 Aberrant activation of anaplastic lymphoma kinase (ALK) has been described in a

159 Aberrant forms of the anaplastic lymphoma kinase (ALK) have been implicated in

160 Analogues structurally related to anaplastic lymphoma kinase (ALK) inhibitor 1 were optimi

161 Ceritinib is a next-generation anaplastic lymphoma kinase (ALK) inhibitor, which has sh

162 Most anaplastic lymphoma kinase (ALK) inhibitors adopt a type

163 that may rationalize clinical evaluation of anaplastic lymphoma kinase (ALK) inhibitors in this sett

164 lending impetus to the development of novel anaplastic lymphoma kinase (ALK) inhibitors with differe

165 naene macrocycles were prepared as potential anaplastic lymphoma kinase (ALK) inhibitors, designed to

166 Anaplastic lymphoma kinase (ALK) is a promising therapeu

167 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine

168 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine

169 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine

170 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine

171 Here we show that the anaplastic lymphoma kinase (ALK) is aberrantly activated

172 The anaplastic lymphoma kinase (ALK) is chromosomally rearra

173 The orphan receptor anaplastic lymphoma kinase (ALK) is one of very few RTKs

174 Here we show that transcription of anaplastic lymphoma kinase (Alk) is repressed by LMO4 in

175 MYCN overexpression combined with activated anaplastic lymphoma kinase (ALK) is sufficient to induce

176 Genetic rearrangements of the anaplastic lymphoma kinase (ALK) kinase occur in 3% to 1

177 ely half of IMTs carry rearrangements of the anaplastic lymphoma kinase (ALK) locus on chromosome 2p2

178 Anaplastic lymphoma kinase (ALK) mutations occur in 3% t

179 malignant transformation of T cells that are anaplastic lymphoma kinase (ALK) negative and CD30 posit

180 The metabolic shift is mediated through the anaplastic lymphoma kinase (ALK) phosphorylation of the

181 The aim of this study is to investigate anaplastic lymphoma kinase (ALK) protein expression and

182 Crizotinib (1), an anaplastic lymphoma kinase (ALK) receptor tyrosine kinas

183 Here we report a novel isoform of the anaplastic lymphoma kinase (ALK) that is expressed in ap

184 aim of the present review is to describe the anaplastic lymphoma kinase (ALK) translocation as a prom

185 sets of lung cancers with EGFR mutations and anaplastic lymphoma kinase (ALK) translocations.

186 h epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit

187 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit

188 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit

189 Anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit

190 ell transformation mediated by the oncogenic anaplastic lymphoma kinase (ALK) tyrosine kinase remain

191 ;5)(p23;q35) results in the juxtaposition of anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM

192 vered in many T-cell malignancies, including anaplastic lymphoma kinase (ALK)(-) anaplastic large cel

193 Genetic studies have established anaplastic lymphoma kinase (ALK), a cell surface recepto

194 a distinct role for one of the DMGs encoding anaplastic lymphoma kinase (ALK), an important regulator

195 se domain that is physiologically related to anaplastic lymphoma kinase (ALK), and is undergoing Phas

196 EGFR), rearranged during transfection (RET), anaplastic lymphoma kinase (ALK), and MAPK1/3 and other

197 ts in nonsmall cell lung cancer fuse EML4 to anaplastic lymphoma kinase (ALK), causing expression of

198 Anaplastic lymphoma kinase (ALK), EGF receptor (EGFR), a

199 otubule-associated protein like 4 (EML4) and anaplastic lymphoma kinase (ALK), generated by an invers

200 Crizotinib, an inhibitor of anaplastic lymphoma kinase (ALK), has also recently show

201 by R1-R6 axons interacts with its receptor, anaplastic lymphoma kinase (Alk), on budding dendrites t

202 Anaplastic lymphoma kinase (ALK), physiologically expres

203 Anaplastic lymphoma kinase (ALK), physiologically expres

204 ), human epidermal growth factor receptor 2, anaplastic lymphoma kinase (ALK), v-Raf murine sarcoma v

205 A gene residing in this locus, the anaplastic lymphoma kinase (Alk), was expressed at signi

206 YCN cooperates with mutational activation of anaplastic lymphoma kinase (ALK), which promotes progres

207 absence of translocations that activate the anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK

208 ied, angioimmunoblastic T-cell lymphoma, and anaplastic lymphoma kinase (ALK)-negative anaplastic lar

209 Anaplastic lymphoma kinase (ALK)-negative anaplastic lar

210 orrelates with relapse risk in children with anaplastic lymphoma kinase (ALK)-positive anaplastic lar

211 Anaplastic lymphoma kinase (ALK)-positive anaplastic lar

212 a small subset of cells purified from human anaplastic lymphoma kinase (ALK)-positive and -negative,

213 ngioimmunoblastic T-cell lymphoma (AITL), 31 anaplastic lymphoma kinase (ALK)-positive and 48 ALK-neg

214 heterogeneous disease that includes systemic anaplastic lymphoma kinase (ALK)-positive and ALK-negati

215 h crizotinib demonstrates robust efficacy in anaplastic lymphoma kinase (ALK)-positive non-small-cell

216 oma, small molecule inhibitor crizotinib for anaplastic lymphoma kinase (ALK)-rearranged inflammatory

217 In a patient who had metastatic anaplastic lymphoma kinase (ALK)-rearranged lung cancer,

218 cacy of ceritinib in patients with untreated anaplastic lymphoma kinase (ALK)-rearranged non-small-ce

219 Most patients with anaplastic lymphoma kinase (ALK)-rearranged or ROS proto

220 eloped as potent and selective inhibitors of anaplastic lymphoma kinase (ALK).

221 scaffold will be described for inhibitors of anaplastic lymphoma kinase (ALK).

222 lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express th

223 noderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion protein is

224 utively active tyrosine kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expressing anaplast

225 he presence of a translocation involving the anaplastic lymphoma kinase ALK gene.

226 p studies, chromosomal rearrangements of the anaplastic lymphoma kinase gene (ALK) have been associat

227 xenograft models of the novel and selective anaplastic lymphoma kinase inhibitor 15b (LDK378) are de

228 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase positive (ALK+) non-small-cel

229 clude the possibility of an EGFR mutation or anaplastic lymphoma kinase translocation or to identify

230 assively parallel sequencing instrument, and anaplastic lymphoma kinase translocation was evaluated b

231 vity to epidermal growth factor receptor and anaplastic lymphoma kinase tyrosine kinase inhibitors ha

232 accompanied by mutational activation of ALK (anaplastic lymphoma kinase), suggesting their pathogenic

233 es the fusion protein NPM-ALK (nucleophosmin-anaplastic lymphoma kinase).

234 t this receptor is expressed on T cells from anaplastic lymphoma kinase-positive (ALK(+)) anaplastic

235 Using conditional transgenic models of anaplastic lymphoma kinase-positive (ALK(+)) lymphomas a

236 Anaplastic lymphoma kinase-positive (ALK+) ALCL is assoc

237 sociated T-cell lymphoma patients (excluding anaplastic lymphoma kinase-positive anaplastic large cel

238 Anaplastic lymphoma kinase-positive anaplastic large-cel

239 d in a caspase-dependent manner in apoptotic anaplastic lymphoma kinase-positive, anaplastic large ce

240 , rare targetable gene fusions involving the anaplastic lymphoma receptor tyrosine kinase (ALK) gene,

241 cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but

242 rotein, NIPA (Nuclear Interacting Partner of Anaplastic Lyphoma Kinase) is linked to a protection fro

243 esmoplastic/nodular and 45.97 for large-cell/anaplastic medulloblastoma) and nonresponse to the first

244 best model for differentiating atypical and anaplastic meningiomas from typical meningiomas consiste

245 SK were significantly higher in atypical and anaplastic meningiomas than in typical meningiomas (P<.0

246 Medulloblastomas that display a large cell/anaplastic morphology and overexpress the cellular c-MYC

247 55) and 40% (95% CI, 0 to 83) for large-cell/anaplastic (n = 5) medulloblastoma ( P < .001 for EFS; P

248 tic oligodendrogliomas, pure (AO) and mixed (anaplastic oligoastrocytoma [AOA]), are chemosensitive,

249 c astrocytoma, anaplastic oligodendroglioma, anaplastic oligoastrocytoma, and brain neoplasm.

250 Adult patients with newly diagnosed anaplastic oligodendroglial tumors were randomly assigne

251 Patients with 1p/19q codeleted anaplastic oligodendroglial tumors who participated in R

252 stine, and vincristine (PCV) chemotherapy in anaplastic oligodendroglial tumors.

253 r 59.4 Gy of RT increases both OS and PFS in anaplastic oligodendroglial tumors.

254 Anaplastic oligodendroglioma (AO) are rare primary brain

255 ocus is often deleted in high-grade gliomas (anaplastic oligodendroglioma and glioblastoma), we inves

256 Anaplastic oligodendroglioma are chemotherapy-sensitive

257 Today, the diagnosis of anaplastic oligodendroglioma requires the presence of bo

258 rapy Oncology Group (RTOG) clinical trial in anaplastic oligodendroglioma suggested a progression-fre

259 patients had glioblastoma multiforme, 2 had anaplastic oligodendroglioma, 1 had anaplastic ependymom

260 a, malignant glioma, anaplastic astrocytoma, anaplastic oligodendroglioma, anaplastic oligoastrocytom

261 de glioma were included: 10 glioblastomas, 1 anaplastic oligodendroglioma, and 1 anaplastic astrocyto

262 ing adult and paediatric glioblastoma (GBM), anaplastic oligodendroglioma, and diffuse intrinsic pont

263 inverse phenomenon was found with grade III anaplastic oligodendrogliomas, in which stronger EGFR ex

264 Anaplastic oligodendrogliomas, pure (AO) and mixed (anap

265 Aggressive thyroid tumors (for example, anaplastic or poorly differentiated thyroid carcinoma) c

266 essing P2X7 exhibited a more tumorigenic and anaplastic phenotype than control cells in vivo, and the

267 CD30+ anaplastic cells in primary cutaneous anaplastic T-cell lymphoma and large-cell transformed cu

268 nd G1 cell-cycle arrest in primary cutaneous anaplastic T-cell lymphoma cells in vitro and a xenograf

269 and antitumor immunity in primary cutaneous anaplastic T-cell lymphoma, and provide a rationale for

270 Primary cutaneous anaplastic T-cell lymphoma, characterized by the CD30+ a

271 toid papulosis (n = 9) and primary cutaneous anaplastic T-cell lymphomas (n = 2) responded; time to r

272 in 97% of patients and poorly differentiated/anaplastic TC in 1.1%.

273 40x10(6)) and human granulocytes (CD56-) or anaplastic thyroid cancer (ARO) cells in the contralater

274 rly differentiated thyroid cancer (PDTC) and anaplastic thyroid cancer (ATC) are rare and frequently

275 Anaplastic thyroid cancer (ATC) is a rare malignancy tha

276 Anaplastic thyroid cancer (ATC) is one of the most letha

277 Anaplastic thyroid cancer (ATC), one of the most aggress

278 In undifferentiated anaplastic thyroid cancer (ATC), we identified two novel

279 mice with characteristic cell morphology of anaplastic thyroid cancer (ATC).

280 Functional investigations using the anaplastic thyroid cancer cell line CAL-62 found that si

281 Anaplastic thyroid cancer is an aggressive and highly le

282 PURPOSE OF REVIEW: Anaplastic thyroid cancer is the most aggressive solid t

283 d two clonal spheroid CSC lines derived from anaplastic thyroid cancer that were even more enriched w

284 patients with pleomorphic xanthoastrocytoma, anaplastic thyroid cancer, cholangiocarcinoma, salivary-

285 ments in normal animals and murine models of anaplastic thyroid cancer, glioblastoma, and triple-nega

286 and expressed at highest levels in PDTC and anaplastic thyroid cancer.

287 oorly differentiated thyroid cancers (PDTC), anaplastic thyroid cancers (ATC), and radioactive iodine

288 p75(NTR) was overexpressed in anaplastic thyroid cancers compared with papillary and f

289 Our study showed that anaplastic thyroid cancers had significantly more CSCs t

290 ge series of human poorly differentiated and anaplastic thyroid cancers screened by next-generation s

291 gher prevalence in poorly differentiated and anaplastic thyroid cancers, and it did not overlap with

292 as in cohorts of patients with medullary and anaplastic thyroid cancers, is presently being done.

293 rum of dedifferentiation from classic PTC to anaplastic thyroid cancers.

294 ct of the proteasome inhibitor bortezomib on anaplastic thyroid carcinoma (ATC) characterized by comp

295 Anaplastic thyroid carcinoma (ATC) has among the worst p

296 Anaplastic thyroid carcinoma (ATC) is a frequently letha

297 Anaplastic thyroid carcinoma (ATC) is one of the most le

298 tance developed in a patient with metastatic anaplastic thyroid carcinoma after an extraordinary 18-m

299 EFS was affected by tumour grade (anaplastic vs differentiated: 2.52 [1.2705.01]; p=0.008)

300 erall survival was affected by tumour grade (anaplastic vs differentiated: HR 3.98 [95% CI 1.51-10.48