ライフサイエンスコーパス: liposarcoma

1 in Fus/TLS (fused in sarcoma/translocated in liposarcoma).

2 ancreas (focal fatty infiltration, teratoma, liposarcoma).

3 stratification for individual patients with liposarcoma.

4 ream targets might lead to novel therapy for liposarcoma.

5 that ZIC1 contributes to the pathogenesis of liposarcoma.

6 y resected locally recurrent retroperitoneal liposarcoma.

7 expression dataset for new drug discovery in liposarcoma.

8 inoma, and breast carcinoma, and 1 recurrent liposarcoma.

9 in patients with high-risk primary extremity liposarcoma.

10 stic for survival in primary retroperitoneal liposarcoma.

11 ies of patients with primary retroperitoneal liposarcoma.

12 stic factors for survival in retroperitoneal liposarcoma.

13 raditionally ascribed to well-differentiated liposarcoma.

14 etus for further study of HDM2 inhibitors in liposarcoma.

15 S patients with a single histopathology, ie, liposarcoma.

16 comparable to that observed in human myxoid liposarcoma.

17 each of the major histologic types of human liposarcoma.

18 eful therapeutic agents for the treatment of liposarcoma.

19 f 44%, higher than previously reported in DD liposarcoma.

20 15 evaluable patients with dedifferentiated liposarcoma.

21 ted pleomorphic sarcoma and dedifferentiated liposarcoma.

22 m surgically resected human dedifferentiated liposarcoma.

23 ated pleomorphic sarcoma or dedifferentiated liposarcoma.

24 y have therapeutic value in dedifferentiated liposarcoma.

25 ase (hTERT) repression in ALT cell lines and liposarcomas.

26 , which falls in a region amplified in human liposarcomas.

27 a as a protein involved in the generation of liposarcomas.

28 mas, rhabdomyosarcomas, chondrosarcomas, and liposarcomas.

29 id tumors, lipomas, uterine leiomyomata, and liposarcomas.

30 romosomes from well- and/or dedifferentiated liposarcomas.

31 ome 12q13-15 that is frequently amplified in liposarcomas.

32 ted in about 75% of FRS2-positive high-grade liposarcomas.

33 aracterize pathologic features of high-grade liposarcomas.

34 ary RPS, the most prevalent histologies were liposarcoma (50%), leiomyosarcoma (26%), and malignant f

35 Here we show that TLS (translocated in liposarcoma), a protein originally identified as the pro

36 Liposarcoma, a rare disease, is classified into five his

37 with postbaseline scans, three patients with liposarcoma achieved a partial response (at 250, 400, an

38 d susceptibility in moderately VSV-resistant liposarcoma and bladder carcinoma.

39 al dacarbazine in patients who have advanced liposarcoma and leiomyosarcoma after they experience fai

40 Liposarcoma and leiomyosarcoma were associated with late

41 factors included the histologic variants of liposarcoma and malignant peripheral nerve tumors and pa

42 ure of oncogene-containing neochromosomes in liposarcoma and provide evidence that they are generated

43 light of the high mortality associated with liposarcoma and the lack of effective systemic therapy,

44 Activation of this receptor in liposarcomas and breast and colon cancer cells also indu

45 in the neoplastic component of human myxoid liposarcomas and increases the tumorigenicity of cells i

46 the q3 weeks 24-hour trabectedin regimen in liposarcomas and leiomyosarcomas, although the qwk 3-hou

47 teins implicated in the development of human liposarcomas and leukemias.

48 FUS/TLS (fused in sarcoma/translocated in liposarcoma) and TDP-43 are integrally involved in amyot

49 % of myxofibrosarcomas and 8% of pleomorphic liposarcomas) and PIK3CA (18% of myxoid/round-cell lipos

50 f normal adipose tissue, well-differentiated liposarcoma, and dedifferentiated liposarcoma by both de

51 fferent human tumor xenografts, melanoma and liposarcoma, and from two normal endothelial cell counte

52 differentiated liposarcoma, dedifferentiated liposarcoma, and leiomyosarcoma.

53 phic sarcoma, two (20%) of ten patients with liposarcoma, and one (10%) of ten patients with synovial

54 vity in mantle-cell lymphoma, breast cancer, liposarcoma, and teratoma with reversible neutropenia as

55 Liposarcomas are aggressive mesenchymal cancers with poo

56 g a novel gene expression strategy, in which liposarcomas are compared to their corresponding adipocy

57 for liposarcoma is surgical excision because liposarcomas are often resistant to traditional chemothe

58 Liposarcomas are rare malignant tumors of adipocytic dif

59 Liposarcomas are the most common type of soft tissue sar

60 etrial stromal sarcoma, and HMGIC fusions in liposarcoma, are discussed.

61 btained from patients with de-differentiated liposarcoma being treated with an inhibitor of the HDM2-

62 plete resection of a primary retroperitoneal liposarcoma between July 1982 and December 2005.

63 not only functions as a tumor suppressor in liposarcoma but also promotes adipogenesis in ASC.

64 erentiated liposarcoma, and dedifferentiated liposarcoma by both deep sequencing of small RNA librari

65 rial for treatment of patients with advanced liposarcoma by using the peroxisome proliferator-activat

66 Liposarcoma can be an aggressive, debilitating, and fata

67 and FUS/TLS (fused in sarcoma/translated in liposarcoma) cause a subset of ALS.

68 Liposarcoma cell differentiation is characterized by acc

69 In the human dedifferentiated liposarcoma cell line (LS141) and the p53 wild-type HCT1

70 ib inhibits growth and induces senescence in liposarcoma cell lines and xenografts.

71 onal genomics to classify a panel of diverse liposarcoma cell lines based on hierarchical clustering

72 liposarcoma compared with normal fat, and in liposarcoma cell lines compared with adipose-derived ste

73 RNAi-mediated knockdown of these genes in liposarcoma cell lines reduced proliferation and invasiv

74 is in dedifferentiated and myxoid/round cell liposarcoma cell lines, but not in either adipose-derive

75 rtant role in the growth of dedifferentiated liposarcoma cell lines.

76 osarcoma samples of all five subtypes and in liposarcoma cell lines.

77 expressed and functional in three high-grade liposarcoma cell lines: FU-DDLS-1, LiSa-2, and SW872.

78 7/8-dependent manner, which in turn promoted liposarcoma cell proliferation, invasion, and metastasis

79 methionine sulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state.

80 sfection of HT1080 (fibrosarcoma) and SW872 (liposarcoma) cell lines and their conditioned media resu

81 ntroduction of miR-193b induced apoptosis in liposarcoma cells and promoted adipogenesis in human adi

82 ogression, identifying communication between liposarcoma cells and their microenvironment as a proces

83 Moreover, primary human liposarcoma cells can be induced to undergo terminal dif

84 ptosis and growth arrest in dedifferentiated liposarcoma cells compared with normal adipocytes.

85 rentiation of normal preadipocytes and human liposarcoma cells in vitro.

86 oring miR-143 expression in dedifferentiated liposarcoma cells inhibited proliferation, induced apopt

87 hat miR-25-3p and miR-92a-3p are secreted by liposarcoma cells through extracellular vesicles and may

88 Expression of miR-193b in liposarcoma cells was downregulated by promoter methylat

89 erodimer, and that simultaneous treatment of liposarcoma cells with both PPAR gamma- and RXR-specific

90 e of all three iPLA2 isoforms in human SW872 liposarcoma cells.

91 nduced G(2)-M growth arrest and apoptosis in liposarcoma cells.

92 d one each of infantile fibrosarcoma, myxoid liposarcoma, cellular congenital mesoblastic nephroma) a

93 omatous samples and shows the feasibility of liposarcoma classification based entirely on gene expres

94 ght to develop a more systematic approach to liposarcoma classification based on gene expression anal

95 Synovial sarcomas, round-cell/myxoid liposarcomas, clear-cell sarcomas and gastrointestinal s

96 in conjunction with histologic features for liposarcoma clinical characterization and lay the ground

97 nt, is overexpressed in all five subtypes of liposarcoma compared with normal fat, and in liposarcoma

98 otein, found in the majority of human myxoid liposarcomas, consists of a fusion between the transcrip

99 Dedifferentiated liposarcoma (DDLPS) is a highly malignant subtype of hum

100 and of the closely related dedifferentiated liposarcoma (DDLPS) subtype, revealed immunohistochemica

101 FRS2 with CDK4 and MDM2 in dedifferentiated liposarcoma (DDLS) and undifferentiated high-grade pleom

102 ated liposarcoma (WDLS) and dedifferentiated liposarcoma (DDLS), both characterized by chromosome 12q

103 l-differentiated (WDLS) and dedifferentiated liposarcomas (DDLS).

104 ominant histologies were well-differentiated liposarcoma, dedifferentiated liposarcoma, and leiomyosa

105 Both lipoma and liposarcoma demonstrated thin septa and regions of incre

106 s subtype that accounts for less than 10% of liposarcoma diagnoses.

107 ts with large, high-grade, primary extremity liposarcoma; DOX is not associated with improved DSS and

108 malignant lesions consisted of scrotal wall liposarcoma, epididymal leiomyosarcoma, and recurrent sp

109 e clinical behavior of myxoid and round-cell liposarcomas, even in neoplasms with few or no round-cel

110 We further show that while angiogenic liposarcomas expand rapidly after inoculation of tumor c

111 All patients who were treated for liposarcoma from July 1, 1982, through July 1, 1998, wer

112 The expression profiles discriminated liposarcoma from normal adipose tissue and well differen

113 utations in Fused in Sarcoma/Translocated in Liposarcoma (FUS) cause familial forms of amyotrophic la

114 ing protein fused in sarcoma/translocated in liposarcoma (FUS) is a novel component of the DNA damage

115 Fused in sarcoma/translated in liposarcoma (FUS/TLS) and TAR DNA-binding protein (TDP)-

116 TDP-43) and fused in sarcoma/translocated in liposarcoma (FUS/TLS) as causative of ALS and FTLD, comb

117 ations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were sp

118 TDP-43 and fused in sarcoma/translocated in liposarcoma (FUS/TLS), and massive accumulation of mitoc

119 DP-43) and fused in sarcoma/translocation in liposarcoma (FUS/TLS), cause an inherited form of ALS th

120 ir gene expression profiles, indicating that liposarcoma gene expression profiles and histologic clas

121 ally expressed genes that may be involved in liposarcoma genesis/progression and serve as potential t

122 In total, 27 patients with liposarcoma had a median progression-free survival of 23

123 ell-differentiated/de-differentiated (WD/DD) liposarcomas has been reported to be minimal, however tr

124 tor in the spectrum of myxoid and round-cell liposarcomas has not been examined.

125 oneal sarcoma and suggest that patients with liposarcoma have a 3-fold higher risk of local recurrenc

126 rates of self renewal, including melanomas, liposarcomas, hepatocellular carcinomas, urothelial carc

127 ment of combined modality treatments against liposarcoma in recent years, a significant proportion of

128 aluated the functions of miRNA (miR-193b) in liposarcoma in vitro and in vivo Deep RNA sequencing on

129 s that were dysregulated in dedifferentiated liposarcomas in both the sequencing and the microarray a

130 ree patients with intermediate to high-grade liposarcomas in whom troglitazone administration induced

131 ant imaging features favoring a diagnosis of liposarcoma included lesion larger than 10 cm (P <.001),

132 several genes amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell p

133 Classification of liposarcoma into subtypes, based on morphologic features

134 Classification of liposarcoma into three biological types encompassing fiv

135 The classification of liposarcomas into four principal subtypes reflects the d

136 omplete resection of primary retroperitoneal liposarcoma is a common clinical problem that frequently

137 ncogenic fusion protein, whereas pleomorphic liposarcoma is a karyotypically complex and especially p

138 Liposarcoma is a type of soft tissue sarcoma that exhibi

139 Myxoid liposarcoma is characterized by a pathognomonic chromoso

140 Because the differentiation status of liposarcoma is predictive of clinical outcomes, modulati

141 Currently, the mainstay of therapy for liposarcoma is surgical excision because liposarcomas ar

142 Well-differentiated liposarcoma is the most common subtype and is associated

143 nce of FRS2 and FGFR signaling in high-grade liposarcomas is unknown.

144 he following histopathologies: fibrosarcoma, liposarcoma, leiomyosarcoma, malignant fibrous histiocyt

145 eiomyomas, Wilms' tumors, rhabdomyosarcomas, liposarcomas, leiomyosarcomas, and adrenal cortical carc

146 Liposarcoma (LPS) can be divided into 4 different subtyp

147 n with dacarbazine in patients with advanced liposarcoma (LPS) or leiomyosarcoma showed a significant

148 DLPS) is a highly malignant subtype of human liposarcoma (LPS), whose genomic profile is characterize

149 Liposarcomas (LPSs) are the most common soft-tissue canc

150 In contrast to extremity liposarcoma, LR without distant metastasis often results

151 rentiation; has tumor suppressor activity in liposarcoma, lung, and prostate cancers; and suppresses

152 to be up-regulated in early growth of human liposarcoma, mammary adenocarcinoma, and osteosarcoma.

153 Here, we use a liposarcoma model system to assay telomere maintenance m

154 Myxoid round cell liposarcoma (MRCLS) is a common liposarcoma subtype char

155 n = 12), six leiomyosarcomas (n = 29), seven liposarcomas (n = 31), three malignant fibrous histiocyt

156 ated genes included TP53 (17% of pleomorphic liposarcomas), NF1 (10.5% of myxofibrosarcomas and 8% of

157 Of 177 patients with primary retroperitoneal liposarcoma operated on for curative intent, 99 (56%) pr

158 the RNA/DNA-binding protein translocated in liposarcoma or fused in sarcoma (TLS/FUS or FUS).

159 versus dacarbazine in patients with advanced liposarcoma or leiomyosarcoma after prior therapy with a

160 th intermediate-grade or high-grade advanced liposarcoma or leiomyosarcoma who had received at least

161 rs previously labeled as well differentiated liposarcomas or atypical lipomas.

162 rcomas) and PIK3CA (18% of myxoid/round-cell liposarcomas, or MRCs).

163 ion (P = 0.01), low-grade tumors (P = 0.02), liposarcomas (P = 0.003), and no disease recurrence (P =

164 analysis of signaling pathways important to liposarcoma pathogenesis and progression in the well-dif

165 correlated with disease-specific survival of liposarcoma patients.

166 novel and previously unreported insight into liposarcoma progression, identifying communication betwe

167 ironment as a process critically involved in liposarcoma progression.

168 Translocation liposarcoma protein (TLS)-associated serine-arginine (TA

169 The translocation liposarcoma protein TLS has recently been shown to funct

170 ways in well-differentiated/dedifferentiated liposarcoma provides several possible novel therapeutic

171 f tumor cells in mice, nonangiogenic dormant liposarcomas remain microscopic up to one-third of the n

172 Liposarcoma remains the most common mesenchymal cancer,

173 Dedifferentiated liposarcoma represents focal progression of well-differe

174 These human xenograft models may facilitate liposarcoma research and accelerate the generation of re

175 d with neural differentiation and round cell liposarcoma, respectively.

176 A 120-day follow-up study of liposarcoma revealed a sustained 2-fold or higher increa

177 and beta-catenin signaling in progression of liposarcoma, revealing mechanistic vulnerabilities that

178 and CHEK1, were found to be overexpressed in liposarcoma samples of all five subtypes and in liposarc

179 ndertook expression profiling of 140 primary liposarcoma samples, which were randomly split into trai

180 but only cells from the nonangiogenic human liposarcoma secrete relatively high levels of the angiog

181 nes, including MYC, as potentially affecting liposarcoma signaling networks and cancer outcome.

182 osine kinase and DNA methylation pathways in liposarcoma, some with immediate implications for therap

183 vel pharmaceutical agents that aim to target liposarcoma-specific biology are under active investigat

184 nografts, and throughout the 120 days of the liposarcoma study.

185 d round cell liposarcoma (MRCLS) is a common liposarcoma subtype characterized by a translocation tha

186 Differentially expressed genes for each liposarcoma subtype compared with normal fat were used t

187 ariate analysis showed that dedifferentiated liposarcoma subtype was associated with a 6-fold increas

188 Several histologically defined liposarcoma subtypes exist, yet little is known about th

189 f a clinical trial with MDM2 antagonists for liposarcoma subtypes which overexpress MDM2 and show the

190 on profiling was able to distinguish between liposarcoma subtypes, lipoma, and normal fat samples.

191 trongly correlates to each of the four major liposarcoma subtypes.

192 lls, including fibrosarcoma, leiomyosarcoma, liposarcoma, synovial sarcoma, and neurofibrosarcoma cel

193 ts with >5 cm, high-grade, primary extremity liposarcoma that underwent surgical treatment of cure fr

194 and a distinct set of genes overexpressed in liposarcomas that are not found in the corresponding sta

195 identified a group of genes overexpressed in liposarcomas that indicate the stage of differentiation

196 tional role in the development of high-grade liposarcomas, therefore, serve as a potential therapeuti

197 ng this with the gene expression profiles of liposarcoma tissue samples, we refined this signature to

198 rmalin-fixed, paraffin-embedded human myxoid liposarcoma tissues, we demonstrate an 80% reduction of

199 The translocation liposarcoma (TLS) gene is fused to the ETS-related gene

200 sarcoma (FUS, also known as translocated in liposarcoma (TLS)) account for approximately 30% of clas

201 Translocated in liposarcoma (TLS), a member of the Ewing's sarcoma famil

202 Human translocation liposarcoma (TLS)-CCAAT/enhancer binding protein (C/EBP)

203 fetal liver cells expressing translocated in liposarcoma (TLS)-ERG, an activated form of ERG found in

204 We find that translocation in liposarcoma (TLS)/FUS, an RNA-binding nuclear protein th

205 ssociated with the differentiation status of liposarcoma to gain insight into the basis for its progr

206 in patients with retroperitoneal (RP) WD/DD liposarcoma treated at The University of Texas MD Anders

207 fy 177 patients with primary retroperitoneal liposarcoma treated between July 1982 and June 2002.

208 In liposarcoma, tumor location exerts as strong an influenc

209 t carcinoma, glioblastoma, osteosarcoma, and liposarcoma tumors.

210 typical lipomatous tumor/well differentiated liposarcoma vs. other).

211 Retroperitoneal dedifferentiated liposarcoma was associated with an 83% local recurrence

212 considered the best predictor of outcome in liposarcoma, was 0.669.

213 % of well-differentiated or dedifferentiated liposarcomas (WD/DDLS) have CDK4 amplification.

214 Well-differentiated liposarcoma (WDLPS), one of the most common human sarcom

215 These include well differentiated liposarcoma (WDLS) and dedifferentiated liposarcoma (DDL

216 Well-differentiated and dedifferentiated liposarcomas (WDLS/DDLS) account for approximately 13% o

217 In myxofibrosarcomas and pleomorphic liposarcomas, we found both point mutations and genomic

218 Seven hundred twenty patients with liposarcoma were evaluated, and of these, 460 had comple

219 Forty-seven cases of myxoid and round-cell liposarcomas were examined.

220 umors (35 lipomas and 25 well-differentiated liposarcomas) were retrospectively reviewed in 31 female

221 Liposarcomas, which are malignant fatty tumors, are the

222 ubset of Ewing's family of tumors and myxoid liposarcomas, which lack one of the characteristic trans

223 he majority of patients with retroperitoneal liposarcoma will eventually have recurrence and die of d

224 tutions influenced LR of well differentiated liposarcoma without impacting OS, whereas discrepancies

225 and FAK inhibitor (PF-562271) each inhibited liposarcoma xenograft growth.